PReD-Bench/PRed-Bench huggingface dataset:
Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me)
Authors: Ping Yue
Zhongmei Zhou
Shi-Yong Sun
Fadlo R Khuri
Journal: Cancer biology & therapy (2006)
Discipline: CLINICAL MEDICINE
Keywords: CDDO-Me; apoptosis; JNK activation; DR5 expression; oxidative stress
Affiliations: Department of Hematology and Oncology, Winship Cancer Institute, Emory University of School of Medicine, Atlanta, Georgia 30322, USA.

Abstract:  The novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me) induces apoptosis in human cancer cells, showing potential as a cancer therapeutic agent. We previously demonstrated that CDDO-Me induces a c-Jun N-terminal kinase (JNK)-mediated DR5 expression and apoptosis. This study revealed the mechanism by which CDDO-Me induces JNK activation and subsequent DR5 upregulation and apoptosis. To determine whether CDDO-Me activates JNK and induces DR5 expression and apoptosis via oxidative stress by inducing the generation of reactive oxygen species (ROS), we examined the effects of various antioxidants on JNK activation, DR5 upregulation, and apoptosis induction by CDDO-Me. Thiol antioxidants, including N-acetyl-L-cycteine (NAC), glutathione (GSH) and dithiothrietol (DTT), abrogated CDDO-Me-induced apoptosis. In contrast, nonthiol antioxidants, including butylated hydroxyanisole (BHA), Trolox, mannitol, and Mn(II) tetra(4-benoic acid) porphyrin chloride (MnTBAP), failed to do so, with the exception of vitamin C (Vit C). Accordingly, only thiol antioxidants blocked JNK activation induced by CDDO-Me. CDDO-Me reduced intracellular levels of GSH; this reduction was abrogated only by thiol antioxidants and Vit C. However, CDDO-Me did not promote ROS generation. These results suggest that depletion of intracellular GSH, but not ROS generation, contributes to CDDO-Me-induced JNK activation and apoptosis, at least in our systems. Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation. Collectively, we conclude that CDDO-Me activates the JNK pathway via depletion of intracellular GSH, leading to DR5 upregulation and induction of apoptosis. 

Retracted: No

PubPeer comments:
 Figure 6. Much more similar than you would expect. https: imgur.com J7gDVz4 , 
 This is really a meticulous work. I will check this issue after the lab reopen if we can locate the original data. These are very old Northern blotting results generated before 2003. Otherwise, the data will be reproduced. We are confident with this finding since it was generated in multiple cell lines. Thanks and stay safe ,
GAS5 promotes myocardial apoptosis in myocardial ischemia-reperfusion injury via upregulating LAS1 expression
Authors: L Xu
X Sun
H-Y Liu
C Chi
S-D Liu
W-X Meng
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: GAS5; cardiomyocyte apoptosis; LAS1; myocardial ischemia-reperfusion injury; H9c2 cells
Affiliations: Department of Cardiovascular Surgery, the First Affiliated Hospital, Harbin Medical University, Harbin, China. .

Abstract:  Objective: This study aims at investigating whether GAS5 (grow arrest-specific 5) could promote cardiomyocyte apoptosis by upregulating LAS1 expression, thereby participating in the development of myocardial ischemia-reperfusion injury. Materials and methods: The expression level of GAS5 in H9c2 cells after hypoxia/reoxygenation (H/R) treatment was detected by quantitative Real time-polymerase chain reaction (qRT-PCR). Myocardial injury markers in H9c2 cells were evaluated using relative commercial kits, including activities of LDH (lactate dehydrogenase), MDA (malondialdehyde), SOD (superoxide dismutase) and GSH-PX (glutathione peroxidase). Cell proliferation and apoptosis were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The protein expressions of apoptosis-related genes and p38/MAPK pathway-related genes were detected by Western blot. The regulatory effects of GAS5 on the p38/MAPK pathway were assessed after treatment with p38/MAPK pathway inhibitor in H9c2 cells. Results: QRT-PCR results showed that the expression levels of GAS5 and LAS1 in H/R-treated H9c2 cells were remarkably upregulated compared to those of controls. GAS5 overexpression increased activities of LDH, MDA, SOD and GSH-PX in H/R-treated H9c2 cells. Meanwhile, GAS5 overexpression reduced cell proliferation and apoptosis of H/R-treated cells. Western blot results suggested that the pro-apoptosis genes Bax and cytochrome C were upregulated, whereas the anti-apoptosis gene Bcl-2 was downregulated after GAS5 overexpression. The overexpression of LAS1 in H9c2 cells obtained the same results as GAS5 overexpression. Furthermore, the expressions of p-p38 and p-ERK were upregulated by GAS5 overexpression. SB203580, the p38/MAPK pathway inhibitor, could reverse the inhibited proliferation and increase apoptosis induced by overexpression of GAS5. Conclusions: GAS5 promotes myocardial apoptosis in myocardial ischemia-reperfusion injury by upregulating LAS1 expression via p38/MAPK pathway. GAS5 may be a potential therapeutic target for myocardial ischemia-reperfusion injury. 

Retracted: No

PubPeer comments:
 The Western blots in this paper look similar to assemblages found in other papers, such as in Weikai Zhang et al., doi: 10.1038 s41417-018-0029-y, https: pubpeer.com publications 84B3D8EA002A6126557F1028305947 or Xian-Qun Chu et al., doi: 10.1016 j.prp.2017.10.003 , https: pubpeer.com publications F1C998AB3F11B5907DE5C45822EE5E For example, a band in the GAPDH panel of Figure 3F looks similar to bands in Chu et al. and Zhang et al. Marked with a red arrow. ![file] Chu et al: ![file] Zhang et al: ![file] ,
Retracted: Autopsy and Histologic Findings of Patients with New Coronavirus Pneumonia: The Pathologic Associations with Hypoxemia
Authors: Jun Zhou
Heng Zhang
Rong Chen
Zhenhua Liu
Xiaochun Fei
Chaofu Wang
Yong Ren
Jun Cai
Ling Yuan
Lei Zhao
Yu Zhang
Journal: Medical Science Monitor (2021)
Discipline: CLINICAL MEDICINE
Keywords: Retraction; Undeclared duplication; Content; Figure images; Previous publication
Affiliations: Department of Pathology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China (mainland)., Department of Pathology, Jin Yin-tan Hospital, Wuhan, Hubei, China (mainland)., Department of Pathology, General Hospital of Central Theater Command, People's Liberation Army (PLA), Wuhan, Hubei, China (mainland)., Department of Pathology, Shanghai Jiaotong University School of Medicine, Shanghai, China (mainland)., Department of Ultrasound, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China (mainland).

Abstract:  This manuscript has been retracted due to the identification of undeclared duplication of content, including Figure images, from a -previous publication by some of the authors: Wang C, Xie J, Zhao L, Fei X, Zhang H, Tan Y, Nie X, Zhou L, Liu Z, Ren Y, Yuan L, Zhang Y, Zhang J, Liang L, Chen X, Liu X, Wang P, Han X, Weng X, Chen Y, Yu T, Zhang X, Cai J, Chen R, Shi ZL, Bian XW. Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. EBioMedicine. 2020; 57: 102833. All authors are requested to declare that manuscripts submitted to this journal are original. This journal makes clear that research fraud of any kind will not be tolerated and will result in immediate retraction. 

Retracted: No

PubPeer comments:
  This manuscript has been retracted due to the identification of undeclared duplication of content, including Figure images, from a u00adprevious publication by some of the authors: Wang C, Xie J, Zhao L, Fei X, Zhang H, Tan Y, Nie X, Zhou L, Liu Z, Ren Y, Yuan L, Zhang Y, Zhang J, Liang L, Chen X, Liu X, Wang P, Han X, Weng X, Chen Y, Yu T, Zhang X, Cai J, Chen R, Shi ZL, Bian XW. Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. EBioMedicine. 2020; 57: 102833.  **All authors are requested to declare that manuscripts submitted to this journal are original. This journal makes clear that research fraud of any kind will not be tolerated and will result in immediate retraction**. ,
Long non-coding RNA SNHG15 accelerates the progression of non-small cell lung cancer by absorbing miR-211-3p
Authors: J Qian
Y-L Xu
X-R Ma
Y Wang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncSNHG15; miR-211-3p; NSCLC; proliferation; migration
Affiliations: Department of Respiratory and Critical Medicine, Beijing Shijitan Hospital, Capital Medical University, Beijing, China. .

Abstract:  Objective: The aim of this study was to investigate whether lncSNHG15 promoted the proliferation and migration of non-small cell lung cancer (NSCLC) cells by binding to miR-211-3p, thereby participating in the development of NSCLC. Patients and methods: Expressions of lncSNHG15 and miR-211-3p in NSCLC tissues and para-cancerous tissues were detected by quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR). LncSNHG15 and miR-211-3p expression in NSCLC cell lines were determined as well. Furthermore, cell counting kit-8 (CCK-8) and transwell assays were performed to evaluate the effects of lncSNHG15 and miR-211-3p on cell proliferation and migration, respectively. The binding relationship between miR-211-3p and ZNF217, as well as between miR-211-3p and lncSNHG15, were further verified by the Luciferase reporter gene assay. In addition, rescue experiments were performed to verify whether lncSNHG15 promoted the proliferation and migration of NSCLC cells by degrading miR-211-3p. Results: The expression of lncSNHG15 in NSCLC tissues was significantly higher than that of para-cancerous tissues. In particular, the expression of lncSNHG15 in NSCLC patients with stage III-IV was higher than those with stage I-II. Furthermore, lncSNHG15 over-expression remarkably promoted the proliferation and migration of NSCLC cells (A549 and H358). The Luciferase reporter gene assay further indicated that lncSNHG15 could bind to miR-211-3p. Simultaneously, miR-211-3p expression in NSCLC tissues was significantly lower than that of para-cancerous tissues. The over-expression of miR-211-3p could inhibit the proliferation and migration of A549 and H358 cells. Meanwhile, the Luciferase reporter gene assay indicated that ZNF217 was the target of miR-211-3p. In addition, the over-expression of ZNF217 reversed the inhibitory effect of miR-211-3p on the proliferative and migratory potentials of A549 and H358 cells. Conclusions: High expression of lncSNHG15 promoted the proliferation and migration of NSCLC cells by upregulating ZNF217 by adsorbing miR-211-3p. 

Retracted: No

PubPeer comments:
 Figure 1.  LncSNHG15 was highly expressed in NSCLC. A, The expression of lncSNHG15 was detected in 24 pairs of paracancerous tissues and lung cancer tissues. The results showed that the expression of lncSNHG15 was significantly higher in lung cancer tissues. B, The expression of lncSNHG15 was markedly higher in NSCLC tissues with stage III-IV than those with stage I-II. The Normal distributions should be the same in 1A and 1B. The lung-cancer distribution in 1A should be the same as the combined I-II and III-IV distributions in 1B. In fact it is hard to see any relationship between them, ![file] ,
Prognostic significance of stathmin expression in correlation with metastasis and clinicopathological characteristics in human ovarian carcinoma
Authors: Xi Wang
Ping Gao
Hui-Zhong Zhang
Fang Lin
San-Hua Wei
Journal: Acta Histochemica (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Stathmin; oncoprotein 18; microtubule-destabilizing proteins; mitosis regulation; gene expression
Affiliations: Department of Clinical Diagnosis, Tangdu Hospital, Fourth Military Medical University, Xinsi Road, 710038 Xi'an, Shaanxi Province, China.

Abstract:  Stathmin, also called oncoprotein 18, is a founding member of the family of microtubule-destabilizing proteins that play a critical role in the regulation of mitosis. Stathmin is non-expressed in normal tissues, but stathmin gene is expressed at high levels in many human malignancies and the relationships between the levels of this gene expression in tumors and prognosis of the patients have been addressed. In this report, we explored the relationships between stathmin mRNA expression in ovarian carcinoma tissues and clinicopathological parameters. We collected and analyzed paraffin wax-embedded ovarian tumor biopsy tissues from 42 ovarian cancer patients in our hospital. We employed RT-PCR method and performed a densitometric analysis to determine the ratio of stathmin relative to beta-actin as an internal marker. Results showed that the stathmin mRNA expression was detected in all the ovarian carcinoma tissue samples and those samples with metastasis had higher levels of stathmin mRNA expression in initial biopsy specimens (P&lt;0.05). Moreover, the levels of stathmin mRNA expression between samples with and without metastasis showed a statistically significant difference (P&lt;0.05). 

Retracted: No

PubPeer comments:
 Figure 2. * Some areas in this photo appear to look repetitive. Shown with boxes of the same color. ![file] , 
 Figure 1. * Pink boxes: The top areas of lanes 2 and 3 look more similar than expected. ![file] ,
MiR-188 inhibits proliferation and promotes apoptosis of lung adenocarcinoma cells by targeting SIX1 to negatively regulate ERK signaling pathway
Authors: Q-Y Guo
D-Q Lv
X-M Wu
H-Y Li
L Lin
S-Q Yan
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-188; proliferation; apoptosis; lung adenocarcinoma; LUAD cells
Affiliations: Department of Respiratory and Critical Medicine, Affiliated Taizhou Hospital of Zhejiang Province of Wenzhou Medical University, Taizhou, China. .

Abstract:  Objective: To explore the effects of micro ribonucleic acid (miR)-188 on proliferation and apoptosis of lung adenocarcinoma (LUAD) cells, and its potential mechanism. Materials and methods: The expression level of miR-188 in LUAD cell lines was detected via quantitative Real Time-Polymerase Chain Reaction (PCR). The effects of miR-188 overexpression on proliferation and apoptosis of A549 cells were detected using methyl thiazolyl tetrazolium (MTT) assay, colony formation assay, and flow cytometry. The potential targets for miR-188 were predicted using the TargetScan Human database, and the interaction between miR-188 and target gene was determined through Dual-Luciferase reporter assay. Moreover, the associations of miR-188 and sine oculis homeobox homolog 1 (SIX1) with the extracellular signal-regulated kinase (ERK) pathway were detected via Western blotting. Results: The expression of miR-188 significantly declined in LUAD cell lines (p&lt;0.05). The overexpression of miR-188 significantly reduced the proliferation rate of A549 cells and increased the percentage of apoptotic A549 cells (p&lt;0.05). Similarly, it was found in colony formation assay that the overexpression of miR-188 inhibited the colony formation ability of A549 cells most significantly (p&lt;0.05). SIX1 was a direct target for miR-188, and its mRNA and protein expressions were downregulated by the overexpression of miR-188. The remarkable downregulation of phosphorylated ERK was observed in A549 cells overexpressing miR-188, while the decline in phosphorylated ERK was reversed in A549 cells overexpressing miR-188 and SIX1. Conclusions: The expression of miR-188 is downregulated in LUAD cell lines. The overexpression of miR-188 inhibits proliferation and promotes apoptosis of LUAD cells, whose functional mechanism may be related to its regulation on the ERK signaling pathway by targeting SIX1. 

Retracted: No

PubPeer comments:
 Figure 3 appears to show some repetitive features, highlighted here with boxes of the same color. ![file] ,
Shaoyao-Gancao Decoction alleviated hyperandrogenism in a letrozole-induced rat model of polycystic ovary syndrome by inhibition of NF-κB activation
Authors: Rui-Gang Hou
Xin-Chun Wang
Jing-Ping Zhang
Yi-Ting Guo
Yao Cheng
Yun-Yun Shao
Jun-Jin Liu
Zhuang-Peng Chang
Xiao-Juan Feng
Journal: Bioscience reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hyperandrogenism; Inflammation; Polycystic ovary syndrome; Shaoyao-Gancao Decoction; nuclear factor kappaB.
Affiliations: Department of Pharmacy, Second Hospital of Shanxi Medical University, Shanxi 030000, China., School of Pharmaceutical, Shanxi Medical University, Shanxi 030000, China., Department of Pharmacy, Second Hospital of Shanxi Medical University, Shanxi 030000, China  .

Abstract:  Shaoyao-Gancao Decoction (SGD) has been widely used for the treatment of gynopathy. The present study aimed to evaluate the therapeutic effect and potential mechanism of SGD on hyperandrogenism in polycystic ovary syndrome (PCOS) rats. In the present work, SGD was orally administrated to the PCOS rats at the dose of 12.5, 25, and 50 g/kg/d for 14 consecutive days. UPLC-MS/MS was performed to identify the main chemical components of SGD. Body weight, ovarian weight, cystic dilating follicles, and serum levels of steroid hormones were tested to evaluate the therapeutic effect of SGD. In order to further clarify the underlying mechanism, we also measured mRNA and the protein levels of NF-κB, NF-κB p65, P-NF-κB p65, and IκB by RT-qPCR and Western blotting techniques. Our results showed that SGD treatment significantly alleviated hyperandrogenism in PCOS rats as evidenced by reduced serum levels of T and increased E2 and FSH levels. In addition, SGD effectively reduced the phosphorylation of NF-κB p65 and increased the expression of IκB. Results of the present study demonstrated that SGD could ameliorate hyperandrogenism in PCOS rats, and the potential mechanism may relate to the NF-κB pathway. 

Retracted: No

PubPeer comments:
 Will the authors be so kind as to post a full uncropped original scan of the Western blot in figure 7A? The B-actin band does not show any background suggesting it may not have originated on the same gel as the others. *** ![file] ,
RAFT1: A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs
Authors: D M Sabatini
M Lui
H Erdjument-Bromage
S H Snyder
P Tempst
Journal: Cell (1994)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: immunosuppressants; rapamycin; FK506; FKBP12; calcineurin

Abstract:  The immunosuppressants rapamycin and FK506 bind to the same intracellular protein, the immunophilin FKBP12. The FKB12-FK506 complex interacts with and inhibits the Ca(2+)-activated protein phosphatase calcineurin. The target of the FKBP12-rapamycin complex has not yet been identified. We report that a protein complex containing 245 kDa and 35 kDa components, designated rapamycin and FKBP12 targets 1 and 2 (RAFT1 and RAFT2), interacts with FKBP12 in a rapamycin-dependent manner. Sequences (330 amino acids total) of tryptic peptides derived from the 245 kDa RAFT1 reveal striking homologies to the yeast TOR gene products, which were originally identified by mutations that confer rapamycin resistance in yeast. A RAFT1 cDNA was obtained and found to encode a 289 kDa protein (2549 amino acids) that is 43% and 39% identical to TOR2 and TOR1, respectively. We propose that RAFT1 is the direct target of FKBP12-rapamycin and a mammalian homolog of the TOR proteins. 

Retracted: No

PubPeer comments:
 Firstly, I would like to illustrate the possible splicing in Figure 3. Of course this is not a concern per se. ![file] However, when you compare Figure 3A and 3B it called my attention that these bands are more similar than expected. Could authors check it please? ![file] An analysis using Forensically ![file] ,
Interpretation of correlated neural variability from models of feed-forward and recurrent circuits
Authors: Rava Azeredo da Silveira
Volker Pernice
Journal: PLoS Computational Biology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Neural populations; correlated variability; network architecture; stimulus discrimination; population codes
Affiliations: Department of Physics, Ecole Normale Supérieure, Paris, France., Laboratoire de Physique Statistique, Ecole Normale Supérieure, PSL Research University; Université Paris Diderot Sorbonne Paris-Cité, Sorbonne Universités UPMC Univ Paris 06; CNRS, Paris, France., Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey, United States of America.

Abstract:  Neural populations respond to the repeated presentations of a sensory stimulus with correlated variability. These correlations have been studied in detail, with respect to their mechanistic origin, as well as their influence on stimulus discrimination and on the performance of population codes. A number of theoretical studies have endeavored to link network architecture to the nature of the correlations in neural activity. Here, we contribute to this effort: in models of circuits of stochastic neurons, we elucidate the implications of various network architectures-recurrent connections, shared feed-forward projections, and shared gain fluctuations-on the stimulus dependence in correlations. Specifically, we derive mathematical relations that specify the dependence of population-averaged covariances on firing rates, for different network architectures. In turn, these relations can be used to analyze data on population activity. We examine recordings from neural populations in mouse auditory cortex. We find that a recurrent network model with random effective connections captures the observed statistics. Furthermore, using our circuit model, we investigate the relation between network parameters, correlations, and how well different stimuli can be discriminated from one another based on the population activity. As such, our approach allows us to relate properties of the neural circuit to information processing. 

Retracted: No

PubPeer comments:
 The first sentence of the intro says it all:  In the search for clues about the function of neural circuits, it **has become customary** to rely upon recordings of the activity of large populations of neurons.  It has become customary. That s all the rationale contemporary neuroscience needs, setting the stage for ad hoc post hoc exercises in futility. And off we go. ,
High molecular weight fibroblast growth factor 2 induces apoptosis by interacting with complement component 1 Q subcomponent-binding protein in vitro
Authors: Xiaobing Hong
Zhanqin Huang
Hongyan Jiang
Zhonglin Chen
Zelin Yu
Yongdong Niu
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: apoptosis; coimmunoprecipitation; complement component 1 Q subcomponent-binding protein; high molecular weight FGF2; mitochondrion.
Affiliations: The Second Affiliated Hospital, Shantou University Medical College, Shantou, China., Department of Pharmacology, Shantou University Medical College, Shantou, China.

Abstract:  Fibroblast growth factor 2 (FGF2) is a multifunctional cell growth factor that regulates cell proliferation, differentiation, adhesion, migration, and apoptosis. FGF2 has multiple isoforms, including an 18-kDa low molecular weight isoform (lo-FGF2) and 22-, 23-, 24-, and 34-kDa high molecular weight isoforms (hi-FGF2). Hi-FGF2 overexpression induces chromatin compaction, which requires the mitochondria and leads to apoptosis. Complement component 1 Q subcomponent-binding protein (C1QBP) plays an important role in mitochondria-dependent apoptosis by regulating the opening of the mitochondrial permeability transition pore. However, the interaction between C1QBP and hi-FGF2 and its role in hi-FGF2-mediated apoptosis remain unclear. Here, we found that hi-FGF2 overexpression induced depolarization of the mitochondrial membrane, cytochrome c release into the cytosol, and a considerable increase in C1QBP messenger RNA and protein expression. Furthermore, coimmunoprecipitation results showed that the mitochondrial protein, C1QBP, interacts with hi-FGF2. C1QBP knockdown using small interfering RNA significantly decreased the localization of hi-FGF2 to the mitochondria and increased the rate of apoptosis. Our results highlight a novel mechanism underlying hi-FGF2-induced, mitochondria-driven cell death involving the direct interaction between hi-FGF2 and C1QBP and the upregulation of C1QBP expression. 

Retracted: No

PubPeer comments:
 Obviously, these figures have been modified FIgure 3B ![file] , 
 Figure 3B appears to have western blot images spliced together: ![file] ,
S100A1 promotes cell proliferation and migration and is associated with lymph node metastasis in ovarian cancer
Authors: Hongyan Chen
Zhen Hua
Jianlin Ma
Zhihua Liu
Tian Tian
Xukun Li
Zhumei Cui
Journal: Discovery medicine (2017)
Discipline: IMMUNOLOGY
Keywords: S100A1; calcium-binding protein; ovarian cancer; expression; clinicopathological parameters
Affiliations: Department of Obstetrics and Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China., These authors contributed equally to this article., State Key Lab of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.

Abstract:  S100A1 is a calcium-binding protein belonging to the family of S100 proteins, and is highly expressed in ovarian cancer. However, its role in ovarian cancer has not yet been fully elucidated. In this study, we examined S100A1 expression in ovarian cancer tissues and normal tissue controls and analyzed the correlation between S100A1 expression and clinicopathological parameters. We found that S100A1 expression was significantly upregulated in ovarian cancer tissues compared with fallopian and normal ovarian epithelium tissues and was significantly associated with lymph node metastasis and International Federation of Gynecology and Obstetrics (FIGO) stages and tumor grades. We then investigated the biological functions of S100A1 in ovarian cancer by cell proliferation, fluorescence-activated cell sorting (FACS), and migration and invasion assays. The results indicated that S100A1 enhanced the ovarian cancer cell proliferation and migration. Together, our findings demonstrated that S100A1 plays an important role in the malignancy of ovarian cancer, and serves as a useful marker for the detection of ovarian malignancy. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have several image overlaps ![file] Note: So far as I can tell, this paper provides no email address for the corresponding authors. Under the  Corresponding Authors heading it gives only this information:  Hongyan Chen, Ph.D., The State Key Laboratory of Molecular Oncology, National Cancer Center Cancer Hospital, Chinese Academy of Medical Sciences, Beijing 100021, China. Zhumei Cui, M.D., The Department of Obstetrics and Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266061, China. Are readers expected to write a letter to correspond? Very unusual for a 2017 paper. ,
Inhibition of PRMT5 suppresses osteoclast differentiation and partially protects against ovariectomy-induced bone loss through downregulation of CXCL10 and RSAD2
Authors: Yuting Wang
Zuowei Lei
Feng Li
Fei Xu
Hanfeng Guan
Anmin Chen
Yonghui Dong
Chao Song
Journal: Cellular signalling (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CXCL10; EPZ015666; Osteoclast; Osteoporosis; PRMT5
Affiliations: Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China., Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Biological Engineering and Regenerative Medicine Center, Department of Orthopedics, Tongji Hospital, Tongji Medical College, HuaZhong University of Science and Technology, Wuhan, Hubei, China. Electronic address: .

Abstract:  Protein arginine methyltransferase 5 (PRMT5) is an arginine methylation methyltransferase that regulates various physiological processes. Abnormal PRMT5 activity has been reported in inflammation and various types of cancers. Because osteoclast differentiation is characterized by the activation of inflammation-related pathways, we speculated that PRMT5 may play a role in this process. In the present study, we found that PRMT5 was upregulated during osteoclast differentiation. Knockdown of PRMT5 with siRNA in bone marrow mononuclear cells (BMMs) resulted in inhibition of receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation. Consistent with the PRMT5 knockdown results, the PRMT5 inhibitor EPZ015666 (EPZ) suppressed osteoclast differentiation and bone resorption. Intraperitoneal administration of EPZ prevented ovariectomy-induced bone loss. Moreover, RANKL-induced NF-κB and MAPK activation was inhibited by EPZ. Expression microarrays showed that the expression of several osteoclast formation-related genes was altered by EPZ treatment, including chemokine C-X-C motif ligand 10 (CXCL10). Administration of recombinant CXCL10 partially reversed the osteoclastogenesis inhibition effect of the PRMT5 inhibitor. Intriguingly, RSAD2, which is a reported antiviral protein, was apparently suppressed when PRMT5 was inhibited. Knockdown of RSAD2 with siRNA in BMMs led to inhibition of osteoclast differentiation. Subsequent ChIP-qPCR identified that both PRMT5 inhibition and knockdown resulted in decreased H3R8 or/and H4R3 methylation at CXCL10 and RSAD2 promotors. In conclusion, our study found that PRMT5 is an activator of osteoclast differentiation and inhibition of PRMT5 partially suppressed osteoclastogenesis through downregulation of CXCL10 and RSAD2. 

Retracted: No

PubPeer comments:
 In Figure 3A, the merged picture does not correspond to the DAPI (blue) and F-Actin (green) staining (RANKL+EPZ). ![file] ,
MicroRNA-22 functions as a tumor suppressor by targeting SIRT1 in renal cell carcinoma
Authors: Yinping Wang
Dongmei Zhang
Shoulin Zhang
Chunguang Yi
Jian Wang
Hongan Wang
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: microRNA-22; renal cell carcinoma; tumor suppressor; SIRT1; proliferation
Affiliations: Internal Medicine Department, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China., Scientific Research Office, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China., College of Pharmacy, Changchun University of Chinese Medicine, Changchun Jingyue National High-Tech Industrial Development Zone, Changchun, Jilin 130117, P.R. China.

Abstract:  Accumulating evidence demonstrates that microRNA-22 (miR-22) was deregulated in many types of cancers and was involved in various cellular processes related to carcinogenesis. However, the exact roles and mechanisms of miR-22 remain unknown in human renal cell carcinoma (RCC). Here, the relationship between miR-22 expression pattern and clinicopathological features of patients with EOC were determined by real-time quantitative RT-PCR (qRT-PCR). Furthermore, the role of miR-22 and possible molecular mechanisms in EOC were investigated by several in vitro approaches and in a nude mouse model. Results from qRT-PCR showed that miR-22 was significantly downregulated in RCC samples compared with corresponding non-cancerous tissues, which was significantly associated with tumor stage and lymph node metastasis. Functional study demonstrated that enforced overexpression of miR-22 in renal cancer cells inhibited proliferation, migration and invasion, and induced cell apoptosis in vitro, and suppressed tumor growth in vivo. In addition, SIRT1 was identified as a direct target of miR-22 by a luciferase reporter assay. Overexpression of miR-22 activated p53 and its downstream target p21 and PUMA, and the apoptosis markers cleaved CASP3 and PARP, and inhibited epithelial-mesenchymal transition (EMT). These findings showed that miR-22 functioned as tumor suppressor in RCC and blocked RCC growth and metastasis by directly targeting SIRT1 in RCC, indicating a potential novel therapeutic role in RCC treatment. 

Retracted: Yes

PubPeer comments:
 Figure 6d Mock and Vector images appear to be identical. *** ![file] , 
 The journal acknowledged this post via social media and linked to this statement on the journalu2019s website. *** ![file] ,
The N-terminus of Paenibacillus larvae C3larvinA modulates catalytic efficiency
Authors: Kayla A Heney
A Rod Merrill
Madison Turner
Journal: Bioscience Reports (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ADP-ribosyltransferase toxins; enzyme mechanisms; honey bee diseases; macrophage cell entry; protein-protein interactions.
Affiliations: Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada, Department of Biochemistry, McGill University, Montreal, Quebec H3G 0B1, Canada

Abstract:  C3larvinA was recently described as a mono-ADP-ribosyltransferase (mART) toxin from the enterobacterial repetitive intergenic consensus (ERIC) III genotype of the agricultural pathogen, Paenibacillus larvae. It was shown to be the full-length, functional version of the previously described C3larvintrunc toxin, due to a 33-residue extension of the N-terminus of the protein. In the present study, a series of deletions and substitutions were made to the N-terminus of C3larvinA to assess the contribution of the α1-helix to toxin structure and function. Catalytic characterization of these variants identified Asp23 and Ala31 residues as supportive to enzymatic function. A third residue, Lys36, was also found to contribute to the catalytic activity of the enzyme. Analysis of the C3larvinA homology model revealed that these three residues were participating in a series of interactions to properly orient both the Q-X-E and S-T-S motifs. Ala31 and Lys36 were found to associate with a structural network of residues previously identified in silico, whereas Asp23 forms novel interactions not previously described. At last, the membrane translocation activity into host target cells of each variant was assessed, highlighting a possible relationship between protein dipole and target cell entry. 

Retracted: No

PubPeer comments:
 An image in figure 5 appears to be repeated. *** ![file] *** False color ![file] ,
A microanalytical capillary electrophoresis mass spectrometry assay for quantifying angiotensin peptides in the brain
Authors: Peter Nemes
Adam P Swiercz
Paul J Marvar
Zhe Yu
Camille Lombard-Banek
Journal: Analytical and Bioanalytical Chemistry (2019)
Discipline: CHEMISTRY
Keywords: Angiotensin; Capillary electrophoresis; High-resolution mass spectrometry; Mouse; Nano-liquid chromatography
Affiliations: Department of Chemistry & Biochemistry, University of Maryland, 8051 Regents Drive, College Park, MD, 20742, USA., Department of Pharmacology & Physiology, Institute for Neuroscience, The George Washington University, 2300 Eye Street NW, Washington, DC, 20037, USA., Department of Chemistry & Biochemistry, University of Maryland, 8051 Regents Drive, College Park, MD, 20742, USA. .

Abstract:  The renin-angiotensin system (RAS) of the brain produces a series of biologically active angiotensinogen-derived peptides involved in physiological homeostasis and pathophysiology of disease. Despite significant research efforts to date, a comprehensive understanding of brain RAS physiology is lacking. A significant challenge has been the limited set of bioanalytical assays capable of detecting angiotensin (Ang) peptides at physiologically low concentrations (2-15 fmol/g of wet tissue) and sufficient chemical specificity for unambiguous molecular identifications. Additionally, a complex brain anatomy calls for microanalysis of specific tissue regions, thus further taxing sensitivity requirements for identification and quantification in studies of the RAS. To fill this technology gap, we here developed a microanalytical assay by coupling a laboratory-built capillary electrophoresis (CE) nano-electrospray ionization (nano-ESI) platform to a high-resolution mass spectrometer (HRMS). Using parallel reaction monitoring, we demonstrated that this technology achieved confident identification and quantification of the Ang peptides at approx. 5 amol to 300 zmol sensitivity. This microanalytical assay revealed differential Ang peptide profiles between tissues that were micro-sampled from the subfornical organ and the paraventricular nucleus of the hypothalamus, important brain regions involved in thirst and water homeostasis and neuroendocrine regulation to stress. Microanalytical CE-nano-ESI-HRMS extends the analytical toolbox of neuroscience to help better understand the RAS. 

Retracted: No

PubPeer comments:
 A Letter to the Editor regarding this publication can be found here: https: pubmed.ncbi.nlm.nih.gov 31709469 ,
Rapid diagnosis of cryptococcal meningitis by microscopic examination of centrifuged cerebrospinal fluid sediment
Authors: H Kuno
Y Sato
K Oizumi
S Osabe
M Kaji
Journal: Journal of the Neurological Sciences (1999)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: India ink test; cryptococcal meningitis; CRAG testing; cerebrospinal fluid; May-Giemsa staining

Abstract:  The classic India ink test is positive in only half of cryptococcal meningitis cases, and reliable, rapid cryptococcal antigen (CRAG) testing requires technical expertise and facilities not always available. We therefore examined cerebrospinal fluid (CSF) sediment using May-Giemsa, periodic acid-Schiff, and Gram stains in 16 patients with cryptococcal meningitis. The India ink test was positive in seven patients (44%), while microscopic examination of sediment revealed cryptococci in 13 (81%); in six of these 13 the India ink test was negative. Both methods failed to detect the pathogen in the remaining three patients. CRAG testing in CSF was negative in two patients (one with acquired immunodeficiency syndrome, one with diabetes mellitus) whose India ink test also was negative while cryptococci were identified in their CSF sediment. No false positives occurred with CSF May-Giemsa staining in 27 cases of aseptic meningitis with negative cultures for Cryptococcus. In all, microscopic examination of centrifuged and stained CSF sediment proved more sensitive for rapid diagnosis of cryptococcal meningitis than the India ink method, and in two of our patients cryptococci were seen in centrifuged CSF sediment despite negative CRAG and India ink tests. 

Retracted: No

PubPeer comments:
 On 14 June 2020 the publisher informed us that this paper was to be retracted. 9 months later, it has not been. Lengthy delays in publication of retraction notices are not in the best interests of readers. , 
 It is now 21 months since Elsevier communicated, via COPE, its undertaking to retract this paper. Recent requests for an update on the retraction to Elsevier, COPE, and the journal did not receive a response. The society associated with the journal, the World Federation of Neurology, responded but was unable to provide any information. ,
Sex differences in p-aminohippuric acid transport in rat kidney: role of membrane fluidity and expression of OAT1
Authors: Adriana M Torres
Nora B Quaglia
Jorgelina A Cerrutti
Anabel Brandoni
Journal: Molecular and Cellular Biochemistry (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Sex differences; kinetic parameters; p-aminohippuric acid; transport; brush border membrane vesicles
Affiliations: Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, CONICET, Argentina.

Abstract:  Sex differences in the kinetic parameters of p-aminohippuric acid (PAH) transport in brush border (BBMV) and basolateral (BLMV) membrane vesicles from kidney cortex have been observed. Membrane fluidity of BBMV was higher in females as compared with male rats as indicated by anisotropy values (0.1897 +/- 0.0010 vs. 0.2003 +/- 0.0014, p &lt; 0.05, for females and males respectively). Membrane fluidity of BLMV were similar in both sexes. Western blot studies revealed that OAT1 protein in female BLMV was present at only 40% of level found in BLMV from male rats. The lower expression of OAT1 in BLMV in association with the higher BBMV fluidity (which may affect the affinity of PAH transporter in this membrane domain) observed in females may be responsible, at least in part, for the gender difference described in renal PAH secretion. 

Retracted: No

PubPeer comments:
 Figure 2. * Red boxes: In the bottom panel, the two lanes look more similar to each other than expected. Part of a set of 60+ papers reported to the journal in October 2015 with a friendly reminder in 2017. In the past five years, the journal did not correct or retract a single paper from this set. ![file] ,
Growth and elongation of axons through mechanical tension mediated by fluorescent-magnetic bifunctional Fe3O4·Rhodamine 6G@PDA superparticles
Authors: Yang Wang
Hao Xu
Yi Liu
Laijin Lu
Jingyan Ren
Ting Liu
Jiayi Zhang
Binxi Li
Shulin Du
Hao Zhang
Journal: Journal of Nanobiotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Axon regeneration; Fe3O4 superparticles; Gene expression profile; Magnetic actuation; Magnetic field

Abstract:  Background: The primary strategy to repair peripheral nerve injuries is to bridge the lesions by promoting axon regeneration. Thus, the ability to direct and manipulate neuronal cell axon regeneration has been one of the top priorities in the field of neuroscience. A recent innovative approach for remotely guiding neuronal regeneration is to incorporate magnetic nanoparticles (MNPs) into cells and transfer the resulting MNP-loaded cells into a magnetically sensitive environment to respond to an external magnetic field. To realize this intention, the synthesis and preparation of ideal MNPs is an important challenge to overcome. Results: In this study, we designed and prepared novel fluorescent-magnetic bifunctional Fe3O4·Rhodamine 6G@polydopamine superparticles (FMSPs) as neural regeneration therapeutics. With the help of their excellent biocompatibility and ability to interact with neural cells, our in-house fabricated FMSPs can be endocytosed into cells, transported along the axons, and then aggregated in the growth cones. As a result, the mechanical forces generated by FMSPs can promote the growth and elongation of axons and stimulate gene expression associated with neuron growth under external magnetic fields. Conclusions: Our work demonstrates that FMSPs can be used as a novel stimulator to promote noninvasive neural regeneration through cell magnetic actuation. 

Retracted: No

PubPeer comments:
  The custom made Fe3O4u00b7Rhodamine 6G@PDA SPs (FMSPs) used in this work are fabricated in-house by coating preassembled Fe3O4u00b7Rhodamine 6G SPs with PDA. HRTEM images show that the FMSPs possess a uniform size with a core size of 50 nm and PDA shell of approximately 10 nm (Fig. 2a, b). Fig 2:  TEM (a) and HRTEM (b) images of FMSPs. ![file] From [Wang et al (2020)] :  The high-resolution transmission electron microscopy (HRTEM) images show that the Fe3O4u00b7R6G@PDA SPs have a uniform size distribution with a Fe3O4u00b7R6G SP core size of 50 nm and a thin PDA shell of about 6.0 nm (Figure 1a,b). ![file] The TEM images appear to show the same particles in these two studies but the HRTEM images and the text specify different PDA shell thickness. I assume that the TEM images are indicative but may not represent the exact formulation used here. , 
 The reused images between different two papers has significantly changed the contrast ![file] , 
 The TEM images in two different papers are identical, however, the contrast has been changed. ![file] , 
 #3 There is uncertainty, then, whether the FMSP has a  PDA shell of approximately **10** nm as in Fig 2(b), or  PDA thicknesses... **15.5** nm as in Fig S2(c). ,
Staphylococcus epidermidis Boosts Innate Immune Response by Activation of Gamma Delta T Cells and Induction of Perforin-2 in Human Skin
Authors: Seth R Thaller
Natasa Strbo
Suzanne Hower
Vivien Chen
Laura Padula
Cheyanne R Head
Gregory V Plano
Olivera Stojadinovic
Jamie L Burgess
Katelyn O&#x27;Neill
Irena Pastar
Denisse Garcia
Marjana Tomic-Canic
Journal: Frontiers in Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Staphylococcus epidermidis; cytotoxicity; gamma delta T cells; human skin; innate immunity
Affiliations: Wound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, United States., Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, United States., Division of Plastic Surgery Dewitt Daughtry, Department of Surgery, University of Miami Miller School of Medicine, Miami, FL, United States.

Abstract:  Perforin-2 (P-2) is an antimicrobial protein with unique properties to kill intracellular bacteria. Gamma delta (GD) T cells, as the major T cell population in epithelial tissues, play a central role in protective and pathogenic immune responses in the skin. However, the tissue-specific mechanisms that control the innate immune response and the effector functions of GD T cells, especially the cross-talk with commensal organisms, are not very well understood. We hypothesized that the most prevalent skin commensal microorganism, Staphylococcus epidermidis, may play a role in regulating GD T cell-mediated cutaneous responses. We analyzed antimicrobial protein P-2 expression in human skin at a single cell resolution using an amplified fluorescence in situ hybridization approach to detect P-2 mRNA in combination with immunophenotyping. We show that S. epidermidis activates GD T cells and upregulates P-2 in human skin ex vivo in a cell-specific manner. Furthermore, P-2 upregulation following S. epidermidis stimulation correlates with increased ability of skin cells to kill intracellular Staphylococcus aureus. Our findings are the first to reveal that skin commensal bacteria induce P-2 expression, which may be utilized beneficially to modulate host innate immune responses and protect from skin infections. 

Retracted: No

PubPeer comments:
 Figure 1B contains a FACS plot duplication: ![file] , 
 **CORRECTION** *In the original article, there was a mistake in Figure 1B as published. The incorrect contour plots for the conditions: Control 24 h and S. epidermidis 48 h were mistakenly included into Figure 1B. The correct representative contour plots in Figure 1B appear below. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.* https: www.frontiersin.org articles 10.3389 fimmu.2021.741437 full ,