PReD-Bench/PRed-Bench huggingface dataset:
NRF2 and HSF1 coordinately regulate heme oxygenase-1 expression
Authors: Hiroshi Kitamura
Takanori Kubo
Shizuka Saito
Sachiye Inouye
Yuta Hatori
Reiko Akagi
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Heat shock factor 1 (HSF1); Heme oxygenase-1 (HO-1); Nuclear factor-erythroid-2-related factor 2 (NRF2); Stress response.
Affiliations: Department of Pharmacy, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University, Japan. Electronic address: ., Department of Pharmacy, Yasuda Women's University, Japan., Department of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, Japan.

Abstract:  Heme oxygenase-1 (HO-1) is an inducible enzyme responding to various stresses and has cytoprotective activities. Although HO-1 has been referred to as heat shock protein (HSP) 32, the heat-mediated induction of HO-1 varies among different species and cell lines. We examined the effects of heat shock on HO-1 expression in mouse embryonic fibroblast (MEF) cells deficient in heat shock factor 1 (HSF1) or nuclear factor-erythroid-2-related factor 2 (NRF2). Heme-induced expression of HO-1 was 2-fold higher in Hsf1-/- cells than in the wild-type cells at both mRNA and protein levels. In Nrf2-/- cells, heme-induced expression of HO-1 was not detected. In contrast, HO-1 expression was markedly induced by heat shock at 40-42 °C in Nrf2-/- cells while the wild-type cells were not responsive. The heat-induced expression of HO-1 in Nrf2-/- cells were almost completely diminished by transfection of siRNA against Hsf1 gene. These results suggest that HSF1 and NRF2 suppress heme-induced and heat-induced HO-1 expression, respectively. 

Retracted: No

PubPeer comments:
 Figure 2C may have a repeated band (red boxes). Could the authors please post the original uncropped scans? I did not look elsewhere. *** ![file] ,
Vitex negundo modulates selenite-induced opacification and cataractogensis in rat pups
Authors: Annie Abraham
B N Rooban
V Sahasranamam
V Sasikala
Journal: Biological Trace Element Research (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: phytochemical therapeutics; Vitex negundo; oxidative stress; in vivo model; Sprague-Dawley rat pups
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, 695581 Kerala, India.

Abstract:  Recently, much interest has been generated in the search for phytochemical therapeutics, as they are largely free from adverse side effects and economical. The goal of this study was to determine the efficacy of Vitex negundo in modulating the selenite-induced oxidative stress in vivo model. Sprague-Dawley rat pups of 8 days old were used for the study and divided into control (G I), selenite induced (G II), and selenite + V. negundo treated (G III). Cataract was induced by the single subcutaneous injection of sodium selenite (4 mg/kg body weight) on the tenth day and V. negundo (2.5 mg/Kg body weight) administered intraperitoneally from eighth to 15th day. Morphological examination of the rat lenses revealed no opacification in G I and mild opacification in G III whereas dense opacification in G II (stages 4-6). Levels of selenium in G II and G III showed no significant changes. The activities of superoxide dismutase, catalase, and Ca(2+)ATPase were significantly increased in G III compared to G II (p &lt; 0.05), while lower level of reactive oxygen species, Ca(2+), and thiobarbituric acid reactive substances were observed in G III compared G II (p &lt; 0.05). These results indicate the therapeutic potential of methanolic extract of V. negundo on modulating biochemical parameters against selenite-induced cataract, which have been reported in this paper for the first time. 

Retracted: No

PubPeer comments:
 Figure 2. One of the photos, representing the eye of a rat induced with selenite and treated with Vitex negundo (Group III), looks remarkably similar to a photo in another paper by this group (V. Sasikala et al., DOI: 10.1089 jop.2010.0049 - https: pubpeer.com publications 6F5D87E7A2495437B6F34EB4F91032) where it represents the eye of a rat induced with selenite and treated with Moringa oleifera leaves . ![file] ,
4-Nonylphenol-enhanced EZH2 and RNF2 expression, H3K27me3 and H2AK119ub1 marks resulting in silencing of p21CDKN1A in vitro
Authors: Biji Chatterjee
Uma Maheswari
Mariyam Athifa
Santosh R Kanade
Krishna Ghosh
Journal: Epigenomics (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 4-nonylphenol (4-NP); BMI1; CDKN1A/p21/WAF1; E2F-1; E3 ubiquitin-protein ligase RING1 (RING1A/RING1B)
Affiliations: Department of Biochemistry & Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala 671316, India, Department of Biochemistry & Molecular Biology, School of Life Sciences, Pondicherry University, Kalapet, Puducherry 605014, India

Abstract:  Aim: To examine the impact of 4-nonylphenol (4-NP), on the expression of polycomb repressive complexes and cellular proliferation. Materials &amp; methods: Cell proliferation assays, quantitative PCR, Western blotting, luciferase reporter assay, chromatin immunoprecipitation-quantitative PCR were used for the study. Results: The 4-NP at 100 nM concentration significantly increased proliferation of MCF-7 cells. It enhanced the expression of RNF2-BMI1 and EZH2-SUZ12 and concomitantly increased H2AK119ub1 and H3K27me3 repressive marks at p21 proximal promoter resulting in its reduced expression. Selective inhibition of RNF2 or EZH2 reverted the 4-NP action. The phospho-CREB, SP1 and E2F-1 are enriched at proximal promoter of RNF2 and EZH2 and cyclin D1, but not p21. Conclusion: The 4-NP-mediated upregulation of RNF2 and EZH2 resulted in epigenetic silencing of p21. 

Retracted: No

PubPeer comments:
 In Figure 2B, part of a Western blot has been duplicated, modified and presented as something else. This is seen by increasing the contrast and comparing the background. Figure 4B and 4F: the actin blot in Figure 4B has been duplicated, modified and presented as something else in Figure 4F. This is seen by increasing the contrast and comparing the background. ![file] ![file] ,
Escheriosome entrapped soluble blood stage antigens impart protective immunity against a multi-drug resistant isolate of Plasmodium yoelii nigeriensis in BALB/c mice
Authors: Anshu Agarwal
Preeti Bajpai
Shailja Misra-Bhattacharya
Deba Farah
Owais Mohammad
Sharad Kumar Sharma
Journal: Vaccine (2006)
Discipline: IMMUNOLOGY
Keywords: Plasmodium yoelii nigeriensis; liposome; vaccine; malaria infection; BALB/c mice

Abstract:  The Plasmodium yoelii nigeriensis murine model was used to evaluate the potential of liposome entrapped soluble blood stage antigens (sAg) based vaccine against malaria infection in BALB/c mice. Results from the present study revealed that immunization with E. coli lipid liposome (escheriosome) entrapped sAg provided strong protective immune responses that successfully suppressed drug resistant strain of Plasmodium yoelii, whereas other forms of sAg such as, egg PC/Chol liposomes entrapped, or its emulsion form with incomplete Freund's adjuvant (IFA) failed to impart significant level of protection. The immune responses, involved with escheriosome-sAg protection, were found to be associated with enhanced antigen specific CD4(+) and CD8(+) T-cell populations. Analysis of cytokine profiles in immunized animals revealed that the protective response was associated with the induction of a Th-1 (IL-2 and IFN-gamma) cells. Furthermore, vaccination with escheriosome entrapped sAg elicited high IgGl and IgG2a isotype response that played important role in imparting protection against blood stage infection of Plasmodium yoelii (MDR) in BALB/c mice. 

Retracted: No

PubPeer comments:
 Figure 7. * Green boxes: Lanes 2 (egg PC liposome entrapped sAg) and 3 (sAg emulsified with Freund s adjuvant) appear to look remarkably similar, except for a differently colored dot around 60 kDa). Could the authors please check? ![file] ,
The Angiogenic Potential of Mesenchymal Stem Cells from the Hair Follicle Outer Root Sheath
Authors: Bernd Lethaus
Alexander K Bartella
Jan-Christoph Simon
Danilo Obradovic
Hanluo Li
Federica Francesca Masieri
Vuk Savkovic
Christian Etz
Rüdiger Zimmerer
Journal: Journal of Clinical Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: MSC; MSCORS; mesenchymal stem cells; mesenchymal stem cells from hair follicle outer root sheath; neoangiogenesis
Affiliations: Department of Oral and Maxillofacial Surgery, Leipzig University Medical Center, 04103 Leipzig, Germany., Department of Cardiology and Angiology, Leipzig Heart Center, 04289 Leipzig, Germany., Biotechnology Unit, Life Sciences, School of (EAST) Engineering, Arts, Science & Technology, University of Suffolk, Ipswich IP41QJ, UK., Department of Dermatology, Venereology and Allergology, Leipzig University Medical Center, 04103 Leipzig, Germany.

Abstract:  Neovascularization is regarded as a pre-requisite in successful tissue grafting of both hard and soft tissues alike. This study considers mesenchymal stem cells from hair follicle outer root sheath (MSCORS) as powerful tools with a neat angiogenic potential that could in the future have wide scopes of neo-angiogenesis and tissue engineering. Autologous MSCORS were obtained ex vivo by non-invasive plucking of hair and they were differentiated in vitro into both endothelial cells and vascular smooth muscle cells (SMCs), two crucial cellular components of vascular grafts. Assessment was carried out by immunostaining, confocal laser-scanning microscopy, gene expression analysis (qRT-PCR), quantitative analysis of anastomotic network parameters, and cumulative length quantification of immunostained α-smooth muscle actin-containing stress fibers (α -SMA). In comparison to adipose mesenchymal stem cells, MSCORS exhibited a significantly higher differentiation efficiency according to key quantitative criteria and their endothelial derivatives demonstrated a higher angiogenic potential. Furthermore, the cells were capable of depositing their own extracellular matrix in vitro in the form of a membrane-cell sheet, serving as a base for viable co-culture of endothelial cells and SMCs integrated with their autologous matrix. Differentiated MSCORS hereby provided a complex autologous cell-matrix construct that demonstrates vascularization capacity and can serve as a base for personalized repair grafting applications. 

Retracted: No

PubPeer comments:
 Figure two appears they have two images which overlap, but are described differently. *** ![file] ,
Specific inhibition of TRPV4 enhances retinal ganglion cell survival in adult porcine retinal explants
Authors: Fredrik Ghosh
Linnéa Taylor
Karin Arnér
Journal: Experimental Eye Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Ganglion cells; Gliosis; Retina; Retinal degeneration; TRPV4.
Affiliations: Department of Ophthalmology, Lund University, SE 22184, Lund, Sweden. Electronic address: ., Department of Ophthalmology, Lund University, SE 22184, Lund, Sweden.

Abstract:  Signaling through the polymodal cation channel Transient Receptor Potential Vanilloid 4 (TRPV4) has been implicated in retinal neuronal degeneration. To further outline the involvement of this channel in this process, we here explore modulation of Transient Receptor Potential Vanilloid 4 (TRPV4) activity on neuronal health and glial activation in an in vitro model of retinal degeneration. For this purpose, adult porcine retinal explants were cultured using a previously established standard protocol for up to 5 days with specific TRPV4 agonist GSK1016790A (GSK), or specific antagonist RN-1734, or culture medium only. Glial and neuronal cell health were evaluated by a battery of immunohistochemical markers, as well as morphological staining. Specific inhibition of TRPV4 by RN-1734 significantly enhanced ganglion cell survival, improved the maintenance of the retinal laminar architecture, reduced apoptotic cell death and attenuated the gliotic response as well as preserved the expression of TRPV4 in the plexiform layers and ganglion cells. In contrast, culture controls, as well as specimens treated with GSK, displayed rapid remodeling and neurodegeneration as well as a downregulation of TRPV4 and the Müller cell homeostatic mediator glutamine synthetase. Our results indicate that TRPV4 signaling is an important contributor to the retinal degeneration in this model, affecting neuronal cell health and glial homeostasis. The finding that pharmacological inhibition of the receptor significantly attenuates neuronal degeneration and gliosis in vitro, suggests that TRPV4 signaling may be an interesting pharmaceutical target to explore for treatment of retinal degenerative disease. 

Retracted: No

PubPeer comments:
 Figure 1A appears to recycling of a processed version of Figure 1A in a earlier publication: https: pubpeer.com publications 459D8F7519C892375C5190F0D10AAC ![file] , 
 We thank the reader for the comment, which for some reason has been published duplicate times . The publisher has been notified and we are in the process of correcting this inadvertent mistake. Best regards, Dr Taylor ,
Intergenerational mentoring, eudaimonic well-being and gene regulation in older adults: A pilot study
Authors: Deena Goldwater
Sharon Stein Merkin
Teresa Seeman
Steven W Cole
Journal: Psychoneuroendocrinology (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Gene expression; Intergenerational; Prosocial behavior; Well-being.
Affiliations: Division of Geriatrics, David Geffen School of Medicine at UCLA, Le Conte Ave, Suite 2339, Los Angeles, CA, 900945-1687, United States. Electronic address: ., Division of Hematology-Oncology, Department of Medicine, Department of Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine at UCLA, 11-934 Factor Bldg, Los Angeles, CA, 90095-1678, United States.

Abstract:  To clarify the biological mechanisms underlying the relationship between pro-social behavior and health, this pilot study examined the impact of a 9-month intergenerational helping intervention on conserved transcriptional response to adversity (CTRA) gene expression profiles, which are characterized by up-regulation of genes involved in inflammation and down-regulation of genes involved in antiviral defenses. The Generation Xchange program trains and places older (age 50+) volunteers in K-3rd grade classrooms to aid students' academic development (reading and math) and address behavioral issues (e.g., inability to focus during class, behaviors that disrupt class). Volunteers were predominately women (89%) and African American (94%) from the neighborhoods around the schools. Repeated measures planned contrast analysis of 53 CTRA indicator transcripts in 50 blood samples collected from 18 individuals on 2-3 occasions revealed a significant reduction in CTRA gene expression from baseline to the average of 3- and 9-month follow-up. The magnitude of individual decrease in CTRA gene expression correlated with the magnitude of individual increase in eudaimonic well-being over time (net of changes in hedonic well-being). In addition to clarifying biological pathways through which pro-social behavior might impact health, these pilot data suggest that the GenX program may have favorable effects on immune cell gene regulation. 

Retracted: No

PubPeer comments:
 Three images in Figure 4F appear to overlap. *** ![file] *** National Natural Science Foundation of China, Grant numbers: 81501982, 81572927, 81672948, 81772794; Jilin Provincial Research Foundation for the Development of Science and Technology Projects, Grant numbers: 20160414005GH, 20170623021TC; Jilin Provincial Industrial Innovation Project, Grant number: 2018C052-7; Jilin University Bethune Plan B Projects, Grant number: 2015222 ,
Induction of heme oxygenase-1 in normal and malignant B lymphocytes by 15-deoxy-Delta(12,14)-prostaglandin J(2) requires Nrf2
Authors: Richard P Phipps
Carolyn J Baglole
Simona Bancos
Irfan Rahman
Journal: Cellular Immunology (2010)
Discipline: IMMUNOLOGY
Keywords: Heme-oxygenase-1; oxidative stress; cytoprotective; anti-inflammatory enzyme; B-lineage cells
Affiliations: Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.

Abstract:  Heme-oxygenase-1 (HO-1) is induced in response to oxidative stress and is believed to be a cytoprotective and anti-inflammatory enzyme. It is unknown whether normal or malignant human B-lineage cells express HO-1. 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) is an interesting electrophilic lipid mediator able to increase oxidative stress in B cells. Here, we tested normal and malignant human B-lineage cells for their ability to express HO-1 in response to 15d-PGJ(2), as well as the signaling pathways required for HO-1 expression. 15d-PGJ(2) potently induced HO-1 protein expression in normal and malignant B cells. Malignant B cells exhibited a greater induction of HO-1 protein compared to normal B lymphocytes. Using siRNA directed against the transcription factor Nrf2 and B cells isolated from Nrf2-deficient mice, we show that HO-1 induction by 15d-PGJ(2) is dependent on Nrf2. These results show that, compared to normal B lymphocytes, malignant B cells have a greater capacity to increase their HO-1 protein levels in response to 15d-PGJ(2). We speculate that the ability to highly express HO-1 by malignant B cells could confer a survival advantage. 

Retracted: No

PubPeer comments:
 Figure 7B. Splice in Cox-2 panel, but not in the other panels. ![file] ,
DDX21 promotes gastric cancer proliferation by regulating cell cycle
Authors: Fulin Chen
Nan Wu
Xin Xie
Yanan Pan
Yu Zhao
Qiuqiu Hou
Yuying Han
Jiayi Cao
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CDK2; Cyclin D1; DEAD (Asp-Glu-Ala-Asp) box helicase 21 (DDX21); Gastric cancer; Proliferation.
Affiliations: Lab of Tissue Engineering, Faculty of Life Science, Northwest University, 229 Taibai North Road, Xi'an, Shaanxi Province, 710069, People's Republic of China. Electronic address: .

Abstract:  DEAD (Asp-Glu-Ala-Asp) cassette helicase 21 (DDX21) is an ATP-dependent RNA helicase that is overexpressed in various malignancies. There is increasing evidence that DDX21 is involved in carcinogenesis and cancer progression by promoting cell proliferation. However, the functional role of DDX21 in gastric cancer is largely unknown. In this study, we observed that DDX21 was significantly up-regulated in gastric cancer tissues compared to paired adjacent normal tissues. The expression of DDX21 was closely related to the pathological stage of gastric cancer. In vitro and in vivo studies had shown that knockdown of DDX21 inhibited gastric cancer cell proliferation, colony formation, G1/S cell cycle transition and xenograft growth, while ectopic expression of DDX21 promoted these cell functions. Mechanically, DDX21 induced gastric cancer cell growth by up-regulating levels of Cyclin D1 and CDK2. Taken together, these results revealed a novel role for DDX21 in the proliferation of gastric cancer cells via the Cyclin D1 and CDK2 pathways. Therefore, DDX21 can be used as a therapeutic target for gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 2B C. Some cells appear to be visible multiple times within the same photo, as marked here with boxes of the same color and shape. ![file] , 
 Figure 5AB. Some cells appear to be visible multiple times within the same photo, as marked here with boxes of the same color and shape. ![file] , 
 Figure 5CD. Some cells appear to be visible multiple times within the same photo, as marked here with boxes of the same color and shape. ![file] ,
Two Coordination Polymers: Protective Activity On Nerve Injury by Increasing miR-219 and Reducing Inflammatory Response
Authors: Li, Guan-Dong
Lai, Sui-Pian
Li, Bing-Hua
Zhan, Yi-An
Liu, Fen
Journal: Journal of Cluster Science (2021)
Discipline: CHEMISTRY
Keywords: transition metal coordination polymers; nerve injury treatment; miR-219; AMPK signaling pathway; inflammatory cytokines

Abstract: Two novel transition metal coordination polymers (CPs) of {Cu(tdc)(Hdmea)2 (1, Hdmea\u2009=\u2009N,N-dimethylethanolamine, tdc\u2009=\u20092,5-thiopenedicarboxylate) and [Co3(H2O)3(tdc)3(dioxane)]·2(dioxane) (2) were prepared via the reaction of Co(NO3)2·6H2O or Cu(NO3)2·3H2O and H2tdc with or without the template reagent Hdmea. The following experiments were carried out to determine the treatment activity for compounds against nerve injury. Firstly, the real time RT-PCR was carried out to determine the miR-219 relative expression in the nerve cells. Then the activation level of the AMPK signaling pathway in the nerve cells was measured with western blot. In addition to this, the ELISA detection was also used in this research, for the inflammatory cytokines’ evaluation. Finally, the inhibition of the compound 1 and compound 2 on the death of the nerve cells was determined with MTT assay.

Retracted: No

PubPeer comments:
  This assessment was carried out totally under the guidance of the instructions with only a little modification. In brief, the normal human nerve cells in the logical growth phage were collected and seeded into the 6 well plates at the final destiny of 10^6 cells per well I would like to know more about the instructions that make it possible for normal human nerve cells to have a logical (logistic?) growth phage (phase?). The authors do not specify the donors of these  normal human nerve cells . This experiment never happened. ,
miR-25-3p promotes proliferation and inhibits autophagy of renal cells in polycystic kidney mice by regulating ATG14-Beclin 1
Authors: Guojian Liu
Rui Yue
Ping Guo
Fanwu Kong
Liting Chen
Yu Shang
Xiaowen Kang
Ruomei Du
Xiyue Wang
Journal: Renal Failure (2020)
Discipline: CLINICAL MEDICINE
Keywords: ATG14; autophagy; miR-25-3p; polycystic kidney disease; proliferation.
Affiliations: Department of Nephrology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China., Department of Respiration, The Second Affiliated Hospital of Harbin Medical, University, Harbin, Heilongjiang, People's Republic of China., Laboratory Department, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang, People's Republic of China.

Abstract:  MicroRNAs are involved in the regulation of the autophagy and proliferation in several diseases. This study aims to verify the role of miR-25-3p in the proliferation and autophagy of renal cells in polycystic kidney disease (PKD). We found that kidney to body weight and blood urea content were increased in PKD mice. Cystic dilations were increased in kidney tissue from PKD mice, and autophagy-related protein ULK1 and the ratio of LC3-II/LC3-I were decreased, indicating autophagy was inhibited in PKD mice. In addition, miR-25-3p was upregulated in PKD mice, and inhibition of miR-25-3p decreased cystic dilations in kidney tissues, increased ULK1 expression and the ratio of LC3-II/LC3-I, indicating inhibition of miR-25-3p enhanced the autophagy in PKD. Besides, inhibition of miR-25-3p suppressed the proliferation of renal cells and downregulated E2F-1 and PCNA expressions. Importantly, miR-25-3p targetedly suppressed ATG14 expression in PKD cells. Finally, silencing ATG14 abolished the inhibition effect of miR-25-3p inhibitor on renal cell proliferation, and reversed the inhibition effect of miR-25-3p inhibitor on E2F-1 and PCNA expressions in in vitro and in vivo experiments, which suggested that ATG14 was involved in the regulation of miR-25-3p-mediated kidney cell proliferation. Therefore, inhibition of miR-25-3p promoted cell autophagy and suppressed cell proliferation in PKD mice through regulating ATG14. 

Retracted: No

PubPeer comments:
 ![file] ![file] ![file] In Figure 1, LC3-1 and LC3-2 should be on the same membrane, using the same antibody, with molecular weights of 16 and 18. There is no way to separate them. Figure 2 has the same problem. Moreover, the rapamycin group appears in the description of Figure 2, but there is no corresponding figure in the figure. I don t know how to use the rapamycin group. ,
Knockdown Of lncRNA NCK-AS1 Regulates Cisplatin Resistance Through Modulating miR-137 In Osteosarcoma Cells
Authors: Xiaofei Shen
Yixin Shen
Minqian Zheng
Yi Cheng
Guoyou Zou
Journal: OncoTargets and therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: NCK1-AS1; cisplatin; drug resistance; miR-137; osteosarcoma.
Affiliations: Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, People's Republic of China., Department of Orthopedics, Yancheng City No.1 People's Hospital, Yancheng 224005, People's Republic of China.

Abstract:  Purpose: Long non-coding RNAs (lncRNAs) have been proved to act crucial parts in the progress of human tumor. However, the role of lncRNAs in drug resistance of tumor cells remains to be further elucidated. The present study aimed to explore whether lncRNA NCK-AS1 could affect the cisplatin (DDP) resistance in human osteosarcoma cell and the underlying molecular mechanism. Methods: The expression of NCK1-AS1 and miR-137 in osteosarcoma cells was detected by qRT-PCR. CCK-8 assay, colony formation assay, Western blotting, wound healing assay and transwell assay were employed to assess the cell proliferation, migration and invasion. In addition, CCK-8 assay, flow cytometry, qRT-PCR and resistance gene activity analysis were performed to assess the DDP sensitivity of osteosarcoma cells. The interaction between NCK1-AS1 and miR-137 was identified using a dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. Results: The results revealed that NCK1-AS1 was significantly upregulated in osteosarcoma cells, as well as in DDP-resistant osteosarcoma cells. NCK1-AS1 silence inhibited the proliferation, migration and invasion of osteosarcoma cells, whereas enhanced the sensitivity of osteosarcoma cells to DDP. Furthermore, NCK1-AS1 directly interacted with miR-137 and overexpression of miR-137 suppressed the proliferation, migration and invasion of osteosarcoma cells. Most importantly, miR-137 overexpression enhanced the sensitivity of osteosarcoma cells to DDP, and high expression of NCK1-AS1 reversed the influences of miR-137 overexpression on DDP-resistant cells. Conclusion: In short, NCK1-AS1 knockdown enhanced DDP sensitivity of osteosarcoma cells by regulating miR-137, which may be a novel potential target for anti-DDP resistance in human osteosarcoma. 

Retracted: No

PubPeer comments:
 Figure3B interestinguff01 ![file] ,
WITHDRAWN: Cardamonin Inhibits Osteoclastogenesis Induced by Tumor Cells Through Interruption of the Signaling Pathway Activated by Receptor Activator of NF-κB Ligand
Authors: Bokyung Sung
Akira Murakami
Bharat B Aggarwal
Sahdeo Prasad
Simone Reuter
Norio Yamamoto
Vivek R Yadav
Journal: Cancer Letters (2011)
Discipline: CLINICAL MEDICINE
Keywords: Article withdrawal; Author; Editor; Publisher; Elsevier Policy
Affiliations: Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.

Abstract:  This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy. 

Retracted: No

PubPeer comments:
 Identified by another reader. Accepted then withdrawn. *** ![file] , 
 ![file] ,
Origin of new emergent Coronavirus and Candida fungal diseases—Terrestrial or cosmic?
Authors: Robyn A Lindley
Edward J Steele
Robert Temple
N Chandra Wickramasinghe
Gensuke Tokoro
Reginald M Gorczynski
Journal: Advances in Genetics (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Candida auris; Coronavirus; Diseases from space; Herd immunity; Pandemics

Abstract:  The origins and global spread of two recent, yet quite different, pandemic diseases is discussed and reviewed in depth: Candida auris, a eukaryotic fungal disease, and COVID-19 (SARS-CoV-2), a positive strand RNA viral respiratory disease. Both these diseases display highly distinctive patterns of sudden emergence and global spread, which are not easy to understand by conventional epidemiological analysis based on simple infection-driven human- to-human spread of an infectious disease (assumed to jump suddenly and thus genetically, from an animal reservoir). Both these enigmatic diseases make sense however under a Panspermia in-fall model and the evidence consistent with such a model is critically reviewed. 

Retracted: No

PubPeer comments:
 In which it is determined that:  The origins and global spread of ... Candida auris ... and SARS-CoV-2 ... display highly distinctive patterns of sudden emergence and global spread, which are not easy to understand by conventional epidemiological analysis based on simple infection-driven human- to-human spread ... Both these enigmatic diseases make sense however under a Panspermia ... model... , 
 Two questions for the authors: 1. u201cSince **global cross-infection over a short timescale ( 1 year) appears very unlikely** one possibility is of independent multiple origins of Candida auris from some widely present Candida ancestor.u201d (emphasis added) Although the authors state global cross-infection is unlikely, I missed the citation or analysis which determined *how unlikely* this global cross-infection could have been. Taking the u201c 1 yearu201d as a given, it still seems a relevant step in proposing an alternative hypothesis to first thoroughly examine known terrestrial mechanisms and assess their probabilities in this case. The authors use of the term u201cunlikelyu201d suggests that they acknowledge that global cross-infections do occur. 2. u201cFurther, from isolates of Candida from four continents Lockhart et al. (2017) did not find C. auris before 2009 confirming that this pathogen was not simply misidentified previously. While there have been claims that earlier isolates of Candida species may also have been Candida auris which were incorrectly identified, these assertions have not been confirmed.u201d This quote from Lockhart et al. (2017) seems to contradict the authors claim above, u201cFour presumed C. haemulonii (the most common misidentification of C. auris) isolates collected before 2009 were retrospectively reidentified as C. auris by using MALDI-TOF mass spectrometry.u201c Could the authors clarify this for me? ,
The angiotensin II type 2 receptor agonist Compound 21 is protective in experimental diabetes-associated atherosclerosis
Authors: Pooja Krishnaswamy
Ulrike M Steckelings
Thomas Unger
Christine Koulis
Terri J Allen
Karin A Jandeleit-Dahm
Mark E Cooper
Bryna S M Chow
Journal: Diabetologia (2016)
Discipline: CLINICAL MEDICINE
Keywords: AT2 receptor; Angiotensin II; Atherosclerosis; Compound 21; Diabetes.
Affiliations: JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetic Complications Division, Baker IDI Heart and Diabetes Research Institute, 75 Commercial Road, P. O. Box 6492, Melbourne, VIC, 3004, Australia., IMM-Department of Cardiovascular and Renal Research, University of Southern Denmark, Odense, Denmark., School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetic Complications Division, Baker IDI Heart and Diabetes Research Institute, 75 Commercial Road, P. O. Box 6492, Melbourne, VIC, 3004, Australia. .

Abstract:  Aims/hypothesis: Angiotensin II is well-recognised to be a key mediator in driving the pathological events of diabetes-associated atherosclerosis via signalling through its angiotensin II type 1 receptor (AT1R) subtype. However, its actions via the angiotensin II type 2 receptor (AT2R) subtype are still poorly understood. This study is the first to investigate the role of the novel selective AT2R agonist, Compound 21 (C21) in an experimental model of diabetes-associated atherosclerosis (DAA). Methods: Streptozotocin-induced diabetic Apoe-knockout mice were treated with vehicle (0.1 mol/l citrate buffer), C21 (1 mg/kg per day), candesartan cilexetil (4 mg/kg per day) or C21 + candesartan cilexetil over a 20 week period. In vitro models of DAA using human aortic endothelial cells and monocyte cultures treated with C21 were also performed. At the end of the experiments, assessment of plaque content and markers of oxidative stress, inflammation and fibrosis were conducted. Results: C21 treatment significantly attenuated aortic plaque deposition in a mouse model of DAA in vivo, in association with a decreased infiltration of macrophages and mediators of inflammation, oxidative stress and fibrosis. On the other hand, combination therapy with C21 and candesartan (AT1R antagonist) appeared to have a limited additive effect in attenuating the pathology of DAA when compared with either treatment alone. Similarly, C21 was found to confer profound anti-atherosclerotic actions at the in vitro level, particularly in the setting of hyperglycaemia. Strikingly, these atheroprotective actions of C21 were completely blocked by the AT2R antagonist PD123319. Conclusions/interpretation: Taken together, these findings provide novel mechanistic and potential therapeutic insights into C21 as a monotherapy agent against DAA. 

Retracted: No

PubPeer comments:
 Some of the bands in Fig. 7b look unexpectedly similar to each other or their reflections. ![file] ,
Coeliac disease: The histology report
Authors: Umberto Volta
Paola Ceppa
Gruppo Italiano Patologi Apparato Digerente (GIPAD)
Società Italiana di Anatomia Patologica e Citopatologia Diagnostica/International Academy of Pathology, Italian division (SIAPEC/IAP)
Vincenzo Villanacci
Enrico Tavani
Carla Vindigni
Journal: Digestive and Liver Disease (2011)
Discipline: CLINICAL MEDICINE
Keywords: intestinal biopsy; coeliac disease; guidelines; morphological evaluation; duodenal biopsy

Abstract:  To this day intestinal biopsy is justly considered the "gold standard" for the diagnosis of coeliac disease (CD). The aim of the authors in setting up these guidelines was to assist pathologists in formulating a more precise morphological evaluation of a duodenal biopsy in the light of clinical and laboratory data, to prepare histological samples with correctly oriented biopsies and in the differential diagnosis with other pathological entities and complications of the disease. A further intention was to promote the conviction for the need of a close collaborative relationship between different specialists namely the concept of a "multidisciplinary team". 

Retracted: No

PubPeer comments:
 These two original papers with multiple data images duplicated. Could the authors explain? See also: https: pubpeer.com search?q=villanacci ![file] , 
 More duplications in these two papers authored by Villanacci V. ![file] , 
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 More duplications by Villanacci V. ![file] , 
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XIST Induced by JPX Suppresses Hepatocellular Carcinoma by Sponging miR-155-5p
Authors: Zhi Ming Huang
Wei Wu
Xiu Qing Lin
Xin Chen
Fang Wu
Journal: Yonsei Medical Journal (2018)
Discipline: CLINICAL MEDICINE
Keywords: JPX; X-chromosome inactivation; XIST; hepatocellular carcinoma; lncRNA
Affiliations: Department of Gastroenterology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Gastroenterology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. .

Abstract:  Purpose: The influence of X-inactive specific transcript (XIST) and X-chromosome inactivation associated long non-coding RNAs (lncRNAs) just proximal to XIST (JPX) on hepatocellular carcinoma (HCC) remains controversial in light of previous reports, which the present study aimed to verify. Materials and methods: The DIANA lncRNA-microRNA (miRNA) interaction database was used to explore miRNA interactions with JPX or XIST. JPX, XIST, and miR-155-5p expression levels in paired HCC specimens and adjacent normal tissue were analyzed by RT-qPCR. Interaction between XIST and miR-155-5p was verified by dual luciferase reporter assay. Expression levels of miR-155-5p and its known target genes, SOX6 and PTEN, were verified by RT-qPCR and Western blot in HepG2 cells with or without XIST knock-in. The potential suppressive role of XIST and JPX on HCC was verified by cell functional assays and tumor formation assay using a xenograft model. Results: JPX and XIST expression was significantly decreased in HCC pathologic specimens, compared to adjacent tissue, which correlated with HCC progression and increased miR-155-5p expression. Dual luciferase reporter assay revealed XIST as a direct target of miR-155-5p. XIST knock-in significantly reduced miR-155-5p expression level and increased that of SOX6 and PTEN, while significantly inhibiting HepG2 cell growth in vitro, which was partially reversed by miR-155-5p mimic transfection. JPX knock-in significantly increased XIST expression and inhibited HepG2 cell growth in vitro or tumor formation in vivo in a XIST dependent manner. Conclusion: JPX and XIST play a suppressive role in HCC. JPX increases expression levels of XIST in HCC cells, which suppresses HCC development by sponging the cancer promoting miR-155-5p. 

Retracted: No

PubPeer comments:
 The authors regret the color of the line segments should be mutually adjusted (in Figure 6b and d). Fig. 6 b and d are replaced by the following figure. ![file] ,
Transforming growth factor-beta regulates stearoyl coenzyme A desaturase expression through a Smad signaling pathway
Authors: Barbara Wiggert
William Samuel
W Tony Parks
Stephen M Prouty
John J Hooks
Joel S Gordon
R Krishnan Kutty
Chandrasekharam N Nagineni
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Stearoyl-CoA desaturase; unsaturated fatty acids; TGF-beta; Smad proteins; lipid metabolism
Affiliations: Biochemistry Section, Laboratory of Retinal Cell and Molecular Biology, NEI, National Institutes of Health, Bethesda, Maryland 20878-2740, USA. 

Abstract:  The regulation of stearoyl-CoA desaturase (SCD), a rate-limiting enzyme in the synthesis of unsaturated fatty acids, is physiologically important because the ratio of saturated to unsaturated fatty acids is thought to control cellular functions by modulating the structural integrity and fluidity of cell membranes. Transforming growth factor-beta (TGF-beta), a multifunctional cytokine, increased SCD mRNA expression in cultured human retinal pigment epithelial cells. This response was elicited by all three TGF-beta isoforms, beta1, beta2, and beta3. However, SCD mRNA expression was not increased either by other members of the TGF-beta family or by other growth factors or cytokines. TGF-beta also increased SCD mRNA expression in several other cell lines tested. The increase in SCD mRNA expression was preceded by a marked increase in Smad2 phosphorylation in TGF-beta-treated human retinal pigment epithelial cells. TGF-beta did not induce SCD mRNA expression in a Smad4-deficient cell line. However, Smad4 overexpression restored the TGF-beta effect in this cell line. Moreover, TGF-beta-induced SCD mRNA expression was effectively blocked by the overexpression of Smad7, an inhibitory Smad. Thus, a TGF-beta signal transduction pathway involving Smad proteins appears to regulate the cellular expression of the SCD gene, and this regulation may play an important role in lipid metabolism. 

Retracted: No

PubPeer comments:
 3. Figure 7. Abnormal splicing tracks (red box) on background of membranes. ![file] , 
 One lane seems to have been replicated throughout the figures in this manuscript. Could the authors review and comment? Figures 1A and 4A shown as examples. *** ![file] *** ![file] ,
miR‑331‑3p suppresses cell invasion and migration in colorectal carcinoma by directly targeting NRP2
Authors: Hongye Zhang
Mingxia Wang
Ruiyu Wang
Journal: Oncology Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: colorectal carcinoma; invasion; miR-331-3p; migration; neuropilin-2.
Affiliations: Department of Oncology, Linyi Central Hospital, Linyi, Shandong 276400, P.R. China

Abstract:  Colorectal carcinoma (CRC) is a common tumor of the digestive system with poor prognosis. Studies have shown that aberrant microRNA (miRNA) expression can affect CRC progression by regulating target genes. In the present study, we investigated the functional roles and potential mechanisms of miR-331-3p in CRC. The expression of miR-331-3p and neuropilin-2 (NRP2) in CRC was detected by RT-qPCR. Then, Transwell assays were conducted to investigate the influence of miR-331-3p on CRC cell invasion and migration abilities. Luciferase reporter assays were performed to determine the target gene of miR-331-3p. It was found that miR-331-3p expression was notably declined in CRC and inversely correlated with the NRP2 expression. miR-331-3p upregulation significantly inhibited CRC cell invasion and migration. Additionally, western blot analysis demonstrated that miR-331-3p restoration evidently suppressed CRC cell EMT. Moreover, NRP2 was conformed to be a novel target of miR-331-3p and knockdown of NRP2 partially inversed the effects of the miR-331-3p inhibitor on cell invasion and migration. These results suggested that miR-331-3p exerted tumor suppressive roles in CRC by targeting NRP2 and miR-331-3p/NRP2 may serve as a potential therapy for CRC. 

Retracted: No

PubPeer comments:
 In Figure 2c, a micrographs has been duplicated and presented as something else. ![file] ,
The Role of KCNMB1 and BK Channels in Myofibroblast Differentiation and Pulmonary Fibrosis
Authors: Steven K Huang
Anne M Scruggs
Gintautas Grabauskas
Journal: American Journal of Respiratory Cell and Molecular Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: IPF; KCNMA1; KCa1.1; MaxiK; fibroblast.
Affiliations: Division of Pulmonary and Critical Care Medicine and., Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan.

Abstract:  The differentiation of fibroblasts into myofibroblasts is critical for the development of fibrotic disorders, including idiopathic pulmonary fibrosis (IPF). Previously, we demonstrated that fibroblasts from patients with IPF exhibit changes in DNA methylation across the genome that contribute to a profibrotic phenotype. One of the top differentially methylated genes identified in our previous study was KCNMB1, which codes for the β subunit of the large-conductance potassium (BK, also known as MaxiK or KCa1.1) channel. Here, we examined how the expression of KCNMB1 differed between IPF fibroblasts and normal cells, and how BK channels affected myofibroblast differentiation. Fibroblasts from patients with IPF exhibited increased expression of KCNMB1, which corresponded to increased DNA methylation within the gene body. Patch-clamp experiments demonstrated that IPF fibroblasts had increased BK channel activity. Knockdown of KCNMB1 attenuated the ability of fibroblasts to contract collagen gels, and this was associated with a loss of α-smooth muscle actin (SMA) expression. Pharmacologic activation of BK channels stimulated α-SMA expression, whereas BK channel inhibitors blocked the upregulation of α-SMA. The ability of BK channels to enhance α-SMA expression was dependent on intracellular calcium, as activation of BK channels resulted in increased levels of intracellular calcium and the effects of BK agonists were abolished when calcium was removed. Together, our findings demonstrate that epigenetic upregulation of KCNMB1 contributes to increased BK channel activity in IPF fibroblasts, and identify a newfound role for BK channels in myofibroblast differentiation. 

Retracted: No

PubPeer comments:
 Supp E2 B+C probably same object (blue boxes). Arrow to fibroblastic foci have different targets (red boxes). ![file] ,
The synaptic accumulation of hyperphosphorylated tau oligomers in Alzheimer disease is associated with dysfunction of the ubiquitin-proteasome system
Authors: Bradley T Hyman
Alberto Serrano-Pozo
Tara L Spires-Jones
Tadafumi Hashimoto
Hwan-Ching Tai
Matthew P Frosch
Journal: American Journal Of Pathology (2012)
Discipline: CLINICAL MEDICINE
Keywords: Alzheimer disease; neurofibrillary tangles; synapses; tau proteins; synaptic dysfunction
Affiliations: MassGeneral Institute of Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Abstract:  In Alzheimer disease (AD), deposition of neurofibrillary tangles and loss of synapses in the neocortex and limbic system each correlate strongly with cognitive impairment. Tangles are composed of misfolded hyperphosphorylated tau proteins; however, the link between tau abnormalities and synaptic dysfunction remains unclear. We examined the location of tau in control and AD cortices using biochemical and morphologic methods. We found that, in addition to its well-described axonal localization, normal tau is present at both presynaptic and postsynaptic terminals in control human brains. In AD, tau becomes hyperphosphorylated and misfolded at both presynaptic and postsynaptic terminals, and this abnormally posttranslationally modified tau is enriched in synaptoneurosomal fractions. Synaptic tau seems to be hyperphosphorylated and ubiquitinated, and forms stable oligomers resistant to SDS denaturation. The accumulation of hyperphosphorylated tau oligomers at human AD synapses is associated with increased ubiquitinated substrates and increased proteasome components, consistent with dysfunction of the ubiquitin-proteasome system. Our findings suggest that synaptic hyperphosphorylated tau oligomers may be an important mediator of the proteotoxicity that disrupts synapses in AD. 

Retracted: No

PubPeer comments:
 Identified by another reader. Earlier correction related to Figure 4B. *** ![file] , 
 Previous correction. https: doi.org 10.1016 j.ajpath.2012.07.035 In the article entitled u201cThe Synaptic Accumulation of Hyperphosphorylated Tau Oligomers in Alzheimer Disease Is Associated With Dysfunction of the Ubiquitin-Proteasome Systemu201d (Volume 181, pages 1426-1435 of the October 2012 issue), Figure 4B, page 1430, contained an error. The authors inadvertently duplicated the bottom right images of Figure 4A, illustrating control synapses, in the right half of panel B, labeled as AD synapses. The correction of the mistake does not alter the conclusions of the article. The corrected Figure 4 (with legend) appears on page 1890. ![file] ,