bluuebunny/crossref_metadata_2025_split huggingface dataset:
The sphingosine 1‐phosphate receptor agonist FTY720 interfered the distribution of dendritic cell and induced the maternal‐fetal immune tolerance
Authors: Xiong Miao , Li Li , Liu Yang , Zhou Fangfang , Shi Nana , Huang Hongling , Wang Jun , Zhu Jieping 
Published: September 2018

AbstractObjectiveThe aim of this study was to investigate the effect of FTY720, an agonist of the sphingosine 1‐phosphate (S1P) receptor, on the embryo loss rate in mice of spontaneous abortion model and the underlying mechanism.MethodsThe effect of intraperitoneal injection of FTY720 on the embryo loss rate in mice of spontaneous abortion model was observed. The expression of S1PR on the dendritic cell (DC) surface was detected by reverse transcription polymerase chain reaction. The quantity and maturation of DCs in peripheral blood and local tissues of pregnant mice, and the expression of CCL19 as well as its receptor C‐C chemokine receptor 7 (CCR7) were detected by flow cytometry and immunohistochemistry. Chemotaxis assay was performed to verify the effect of FTY720 on the chemotaxis of DCs.Results(1) FTY720 had no significant effect on the embryo loss rate in normal pregnant rats. In contrast, adoptive transferring of FTY720 significantly reduced the embryo loss rate of the spontaneous abortion mouse model (P < 0.05). (2) S1PR was extensively expressed on DC surface. The S1P receptor agonist FTY720 reduced the expressions of DC surface chemokines and its receptor (P < 0.05), resulting in a significant reduction in the number of DCs that were chemoattracted to maternal‐fetal interface flow cytometry (P < 0.05). (3) FTY720 had no significant effect on the differentiation and apoptosis rate of DCs (P > 0.05).ConclusionWe hypothesized that FTY720 may reduce the number of DCs that were chemoattracted to the maternal‐fetal interface by downregulating the expression of CCR7, which ultimately induces maternal‐fetal immune tolerance.
Interaction of estrogen receptor β5 and interleukin 6 receptor in the progression of non–small cell lung cancer
Authors: Tang Hexiao , Bai Yuquan , Xiong Lecai , Zhang Li , Wei Yanhong , Zhu Minglin , Wu Xiaoling , Long Ding , Yang Junhui , Yu Li , Xu Shufang , Zhao Jinping 
Published: September 2018

AbstractNumerous studies have shown that the estrogen receptor beta (ERβ) and interleukin 6 receptor (IL‐6R) had interaction in many tumors, including lung cancer. Previous studies found that ERβ5 exhibits a different biological function compared with the other subtypes of ERβ. Therefore, this study mainly explores the interaction between ERβ5 and IL‐6R in the progression of lung cancer. We found that the expression of ERβ5, IL‐6 and glycoprotein 130 (GP130) were significantly increased (P < 0.001) and the 5‐year survival rate with the co‐expression of ERβ5 and GP130 is significantly lower (P = 0.0315) in non‐small cell lung cancer (NSCLC) patients. The cell proliferation, invasion, and cell cycle were markedly increased, and the cell apoptotic was markedly inhibited with the concurrent action of ERβ5 and IL‐6 in A549 cells (P < 0.05). In addition, the expression of ERβ5, GP130, p‐AKT, and p‐44/42 MAPK was also significantly increased in A549 cells (P < 0.05). These results indicate that ERβ5 and GP130 can synergistically promote the progression of NSCLC and maybe combined as an independent prognostic factor in patients. In addition, these results also provide a theoretical basis for the combined targeting therapy of ERβ5 and GP130 in NSCLC.
High levels of methionine and methionine sulfoxide: Impact on adenine nucleotide hydrolysis and redox status in platelets and serum of young rats
Authors: Soares Mayara Sandrielly Pereira , da Silveira de Mattos Bruna , Ávila Anita Almeida , Spohr Luiza , Pedra Nathalia Stark , Teixeira Fernanda Cardoso , Bona Natália Pontes , Oliveira Pathise Souto , Stefanello Francieli Moro , Spanevello Roselia Maria 
Published: September 2018

AbstractWe investigated acute and chronic effects administration of methionine (Met) and/or methionine sulfoxide (MetO) on ectonucleotidases and oxidative stress in platelets and serum of young rats. Wistar rats were divided into four groups: control, Met, MetO, and Met + MetO. In acute treatment, the animals received a single subcutaneous injection of amino acid(s) and were euthanized after 1 and 3 hours. In chronic protocol, Met and/or MetO were administered twice a day with an 8‐hour interval from the 6th to the 28th day of life. Nucleoside triphosphate phosphohydrolase and 5′‐nucleotidase activities were reduced in platelets and serum by Met, MetO, and Met + MetO after 3 hours and 21 days. Adenosine deaminase activity reduced in platelets at 3 hours after MetO and Met + MetO administration and increased after 21 days in animals treated with Met + MetO. Superoxide dismutase and catalase activities decreased in platelets in MetO and Met + MetO groups after 3 hours, while reactive oxygen species (ROS) levels increased in same groups. Catalase activity in platelets decreased in all experimental groups after chronic treatment. Met, MetO, and Met + MetO administration increased plasmatic ROS levels in acute and chronic protocols; glutathione
S‐transferase activity increased by MetO and Met + MetO administration at 3 hours, and ascorbic acid decreased in all experimental groups in acute and chronic protocols. Thiobarbituric acid reactive substances increased, superoxide dismutase and catalase activities reduced in the Met and/or MetO groups at 3 hours and in chronic treatment. Our data demonstrated that Met and/or MetO induced changes in adenine nucleotide hydrolysis and redox status of platelets and serum, which can be associated with platelet dysfunction in hypermethioninemia.
Methotrexate chemotherapy–induced damages in bone marrow sinusoids: An in vivo and in vitro study
Authors: Hassanshahi Mohammadhossein , Su Yu‐Wen , Fan Chia‐Ming , Khabbazi Samira , Hassanshahi Alireza , Xian Cory J. 
Published: September 2018

AbstractChemotherapeutic agents are very well evident extrinsic stimuli for causing damage to endothelial cells. Methotrexate is an antimetabolite commonly used to treat solid tumours and paediatric cancers. However, studies on the effect(s) of methotrexate on bone marrow microvascular system are inadequate. In the current study, we observed a significant bone marrow microvascular dilation following methotrexate therapy in rats, accompanied by apoptosis induction in bone marrow sinusoidal endothelial cells, and followed by recovery of bone marrow sinusoids associated with increased proliferation of remaining bone marrow sinusoidal endothelial cells. Our in vitro studies revealed that methotrexate is cytotoxic for cultured sinusoidal endothelial cells and can also induce apoptosis which is associated with upregulation of expression ratio of Bax and
Bcl‐2 genes and
Bax/Bcl‐2 expression ratio. Furthermore, it was shown that methotrexate can negatively affect proliferation of cultured sinusoidal endothelial cells and also inhibit their abilities of migration and formation of microvessel like tubes. The data from this study indicates that methotrexate can cause significant bone marrow sinusoidal endothelium damage in vivo and induce apoptosis and inhibit proliferation, migration and tube‐forming abilities of sinusoidal endothelial cells in vitro.
Knockdown of RPL34 inhibits the proliferation and migration of glioma cells through the inactivation of JAK/STAT3 signaling pathway
Authors: Ji Peigang , Wang Liang , Liu Jinghui , Mao Ping , Li Ruichun , Jiang Haitao , Lou Miao , Xu Meng , Yu Xiao 
Published: September 2018

AbstractRibosomal protein L34 (RPL34), belonging to the L34E family of ribosomal proteins, was reported to be dysregulated in several types of cancers and plays important roles in tumor progression. However, the expression and roles of RPL34 in human glioma remain largely unknown. Thus, the objective of this study was to investigate the expression and role of RPL34 in glioma. We report here that RPL34 is highly expressed in human glioma tissues and cell lines. Knockdown of RPL34 markedly inhibited the proliferation, migration, and invasion, as well as prevented the epithelial‐mesenchymal transition phenotype in glioma cells. Further, mechanistic analysis showed that knockdown of RPL34 significantly downregulated the levels of p‐JAK and p‐STAT3 in glioma cells. Taken together, our findings indicated that knockdown of RPL34 inhibits the proliferation and migration of glioma cells through the inactivation of JAK/STAT3 signaling pathway. Thus, RPL34 may serve as a potential therapeutic target for the treatment of glioma.
Sodium selenite induces apoptosis via ROS‐mediated NF‐κB signaling and activation of the Bax–caspase‐9–caspase‐3 axis in 4T1 cells
Authors: Zhang Tao , Zhao Gan , Zhu Xinying , Jiang Kangfeng , Wu Haichong , Deng Ganzhen , Qiu Changwei 
Published: September 2018

AbstractSodium selenite (SSE), a source of inorganic selenium, has been widely used as a clinical cancer treatment, but the precise molecular mechanisms of SSE remain to be elucidated. Our in vitro experiments have confirmed that SSE treatment causes a transient increase in intracellular reactive oxygen species (ROS) levels, resulting in the inhibition of nuclear transcription factor‐κB (NF‐κB) signaling and p65 and nuclear factor of kappa light polypeptide gene enhancer in B‐cells inhibitor, alpha phosphorylation levels in 4T1 cells. The inhibition of NF‐κB subsequently increased the expression of the apoptosis gene B‐cell lymphoma‐2‐associated X (Bax) and downregulated the transcription of antiapoptosis genes, such as B‐cell lymphoma‐2, cellular inhibitor of apoptosis 1, and X‐linked inhibitor of apoptosis. Additionally, the accumulation of ROS caused mitochondrial dysfunction, leading to the activation of caspase‐9 and ‐3, thereby resulting in apoptosis. However, modulation of the ROS level by the chemical inhibitor N‐acetyl‐cysteine reversed these events. Similarly, in vitro murine syngeneic breast tumor models showed that SSE inhibits tumor growth by promoting apoptosis. These results indicate that SSE induces apoptosis via ROS‐mediated inhibition of NF‐κB signaling and activation of the Bax–caspase‐9–caspase‐3 axis.
Downregulated miR‐187 contributes to the keratinocytes hyperproliferation in psoriasis
Authors: Tang Lipeng , He Songmin , Zhu Ying , Feng Bing , Su Zuqing , Liu Bo , Xu Fangfang , Wang Xieqi , Liu Hongying , Li Chutian , Zhao Jie , Zheng Xirun , Li Caiyun , Sun Chaoyue , Lu Chuanjian , Zheng Guangjuan 
Published: September 2018

AbstractPsoriasis is a common chronic skin disease characterized by epidermal hyperplasia and inflammation. However, the pathogenesis of psoriasis is multifactorial and is not fully understood. MicroRNAs (miRNAs) represent a promising class of small, noncoding RNA molecules that have a large impact on cellular functions by regulating gene expression. Here we reported that microRNA‐187 (miR‐187), which is one of the most dynamic microRNAs identified in the deep screening miRNAs profile, is downregulated in inflammatory cytokines‐stimulated keratinocytes and psoriatic skins. By luciferase activity assay and gain‐of‐function studies, we showed that miR‐187 inhibits keratinocytes hyperproliferation by targeting CD276. Moreover, overexpression of miR‐187 decreases acanthosis and reduces the disease severity in psoriasis mouse models. Taken together, the results of our study implies miR‐187 as a critical factor in psoriasis pathogenesis, which could be a potent target for psoriasis treatment.
Mitochondrial inner membrane protein, Mic60/mitofilin in mammalian organ protection
Authors: Feng Yansheng , Madungwe Ngonidzashe B. , Bopassa Jean C. 
Published: September 2018

AbstractThe identification of the mitochondrial contact site and cristae organizing system (MICOS) in the inner mitochondrial membrane shed light on the intricate components necessary for mitochondria to form their signature cristae in which many protein complexes including the electron transport chain are localized. Mic60/mitofilin has been described as the core component for the assembly and maintenance of MICOS, thus controlling cristae morphology, protein transport, mitochondrial DNA transcription, as well as connecting the inner and outer mitochondrial membranes. Although Mic60 homologs are present in many species, mammalian Mic60 is only recently gaining attention as a critical player in several organ systems and diseases with mitochondrial‐defect origins. In this review, we summarize what is currently known about the ever‐expanding role of Mic60 in mammals, and highlight some new studies pushing the field of mitochondrial cristae organization towards potentially new and exciting therapies targeting this protein.
Methylene blue offers neuroprotection after intracerebral hemorrhage in rats through the PI3K/Akt/GSK3β signaling pathway
Authors: Chen Chunli , Zhou Fangfang , Zeng Liuwang , Jiang Zheng , Hu Zhiping 
Published: September 2018

AbstractInflammation and apoptosis are two key factors contributing to secondary brain injury after intracerebral hemorrhage (ICH). In the present study, we explored the neuroprotective role of methylene blue (MB) in ICH rats and studied the potential mechanisms involved. Rats were subjected to local injection of collagenase IV in the striatum or sham surgery. We observed that MB treatment could exert a neuroprotective effect on ICH by promoting neurological scores, decreasing the brain water content, alleviating brain–blood barrier disruption, and improving the histological damages in the perihematomal areas. Furthermore, we demonstrated that the various mechanisms underlying MB’s neuroprotective effects linked to inhibited apoptosis and inhibited neuroinflammation. In addition, wortmannin, a selective inhibitor of phosphoinositide 3‐kinase (PI3K), could reverse the antiapoptotic and anti‐inflammatory effects of MB, which suggested that the PI3K–Akt pathway played an important role. In conclusion, these data suggested that MB could inhibit apoptosis and ameliorate neuroinflammation after ICH, and its neuroprotective effects might be exerted via the activation of the PI3K/Akt/GSK3β pathway.
Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment
Authors: González‐Sánchez Jessica , Sánchez‐Temprano Agustín , Cid‐Díaz Tania , Pabst‐Fernández Regina , Mosteiro Carlos S. , Gallego Rosalía , Nogueiras Ruben , Casabiell Xesús , Butler‐Browne Gillian S. , Mouly Vincent , Relova José Luis , Pazos Yolanda , Camiña Jesús P. 
Published: September 2018

AbstractBackgroundThis study was performed to test the therapeutic potential of obestatin, an autocrine anabolic factor regulating skeletal muscle repair, to ameliorate the Duchenne muscular dystrophy (DMD) phenotype.Methods and resultsUsing a multidisciplinary approach, we characterized the ageing‐related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4‐, 8‐, and 18‐week‐old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8‐week‐old mdx mice (n = 5/group). The findings were extended to in vitro effects on human immortalized DMD myotubes. An analysis of TAs revealed an age‐related loss of preproghrelin expression, as precursor of obestatin, in mdx mice. Administration of obestatin resulted in a significant increase in tetanic specific force (33.0% ± 1.5%, P < 0.05), compared with control mdx mice. Obestatin‐treated TAs were characterized by reduction of fibres with centrally located nuclei (10.0% ± 1.2%, P < 0.05) together with an increase in the number of type I fibres (25.2% ± 1.7%, P < 0.05) associated to histone deacetylases/myocyte enhancer factor‐2 and peroxisome proliferator‐activated receptor‐gamma coactivator 1α axis, and down‐regulation of ubiquitin E3‐ligases by inactivation of FoxO1/4, indexes of muscle atrophy. Obestatin reduced the level of contractile damage and tissue fibrosis. These observations correlated with decline in serum creatine kinase (58.8 ± 15.2, P < 0.05). Obestatin led to stabilization of the sarcolemma by up‐regulation of utrophin, α‐syntrophin, β‐dystroglycan, and α7β1‐integrin proteins. These pathways were also operative in human DMD myotubes.ConclusionsThese results highlight the potential of obestatin as a peptide therapeutic for preserving muscle integrity in DMD, thus allowing a better efficiency of gene or cell therapy in a combined therapeutic approach.
Bisphenol A affects neural development of the ascidian Ciona robusta
Authors: Messinetti Silvia , Mercurio Silvia , Pennati Roberta 
Published: September 2018

AbstractBisphenol A (BPA) is an organic pollutant derived from plastic degradation that has numerous and variable adverse effects on human health and wildlife. In particular, it has been reported that BPA can alter reproductive processes and nervous system development in vertebrates. Considering BPA presence in marine environment and the scant data available on its interaction with nervous system development, we analyzed the effect of BPA exposure on sperm viability, fertilization, embryogenesis, and neural differentiation of the ascidian Ciona robusta. Ascidians are members of the Phylum Tunicata, the sister group of Vertebrata, sharing with them fundamental developmental processes. Our results showed that first cell division was altered starting from 5 µM concentration. Lethal concentration (LC
50) was estimated to be 5.2 µM. Larvae developed from treated embryos showed specific malformations to the pigment cells even at 0.1 µM, corresponding to the highest environmental concentration reported so far. Moreover, GABAergic and dopaminergic neurons proved to be target organs of BPA teratogenic action, in accordance with similar results reported in vertebrate animal models. Overall, our results suggest that BPA can exert its effects on nervous system acting on different pathways and underline that
C. robusta is a valuable invertebrate animal model for preliminary screenings of effects of pollutants on vertebrates.
Frequency Offset Corrected Inversion Pulse for B0 and B1 Insensitive Fat Suppression at 3T: Application to MR Neurography of Brachial Plexus
Authors: Wang Xinzeng , Greer Joshua S. , Dimitrov Ivan E. , Pezeshk Parham , Chhabra Avneesh , Madhuranthakam Ananth J. 
Published: September 2018

BackgroundThe 3D short tau inversion recovery (STIR) sequence is routinely used in clinical MRI to achieve robust fat suppression. However, the performance of the commonly used adiabatic inversion pulse, hyperbolic secant (HS), is compromised in challenging areas with increased B0 and B1 inhomogeneities, such as brachial plexus at 3T.PurposeTo demonstrate the frequency offset corrected inversion (FOCI) pulse as an efficient fat suppression STIR pulse with increased robustness to B0 and B1 inhomogeneities at 3T, compared to the HS pulse.Study TypeProspective.Subjects/PhantomInitial evaluation was performed in phantoms and one healthy volunteer by varying the B1 field, while subsequent comparison was performed in three healthy volunteers and five patients without varying the B1.Field Strength/Sequence3T; 3D TSE‐STIR with HS and FOCI pulses.AssessmentBrachial plexus images were qualitatively evaluated by two musculoskeletal radiologists independently using a four‐point grading scale for fat suppression, shading artifacts, and nerve visualization.Statistical TestThe Wilcoxon signed‐rank test with P < 0.05 was considered statistically significant.ResultsSimulations and phantom experiments demonstrated broader bandwidth (2.5 kHz vs. 0.83 kHz, increased B0 robustness) at the same adiabatic threshold and lower adiabatic threshold (5 μT vs. 7 μT at 3.5 ppm, increased B1 robustness) at the same bandwidth with the FOCI pulse compared to the HS pulse With increased bandwidth, the FOCI pulse achieved robust fat suppression even at 50% of maximum B1 strength, while the HS pulse required >75% of maximum B1 strength. Compared to the standard 3D TSE‐STIR with HS pulse, the FOCI pulse achieved uniform fat suppression (P < 0.05), better nerve visualization (P < 0.05), and minimal shading artifacts (P < 0.01) in brachial plexus at 3T.Data ConclusionThe FOCI pulse has increased robustness to B0 and B1 inhomogeneities, compared to the HS pulse, and enables uniform fat suppression in brachial plexus at 3T.Level of Evidence: 1Techinical Efficacy: Stage 1J. Magn. Reson. Imaging 2018;48:1104–1111.
Red nucleus interleukin‐1β evokes tactile allodynia through activation of JAK/STAT3 and JNK signaling pathways
Authors: Guo Yi‐Jie , Li Hao‐Nan , Ding Cui‐Ping , Han Shui‐Ping , Wang Jun‐Yang 
Published: September 2018

AbstractWe previously reported that interleukin‐1β (IL‐1β) in the red nucleus (RN) is involved in pain modulation and exerts a facilitatory effect in the development of neuropathic pain. Here, we explored the actions of signaling pathways, including the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3), c‐Jun N‐terminal kinase (JNK), extracellular signal‐regulated kinase (ERK), p38 mitogen‐activated protein kinase (p38 MAPK) and nuclear factor‐κB (NF‐κB) pathways, on RN IL‐1β‐mediated pain modulation. After a single dose of recombinant rat IL‐1β (rrIL‐1β, 10 ng) injected into the RN in normal rats, a tactile allodynia was evoked in the contralateral but not ipsilateral hindpaw, commencing 75 min and peaking 120 min postinjection. Up‐regulated protein levels of phospho‐STAT3 (p‐STAT3) and p‐JNK were observed in the RN 120 min after rrIL‐1β injection, the increases of p‐STAT3 and p‐JNK were blocked by anti‐IL‐1β antibody. However, the expression levels of p‐ERK, p‐p38 MAPK, and NF‐κB in the RN were not affected by rrIL‐1β injection. RN neurons and astrocytes contributed to IL‐1β‐evoked up‐regulation of p‐STAT3 and p‐JNK. Further studies demonstrated that injection of the JAK2 antagonist AG490 or JNK antagonist SP600125 into the RN 30 min prior to the administration of rrIL‐1β could completely prevent IL‐1β‐evoked tactile allodynia, while injection of the ERK antagonist PD98059, p38 MAPK antagonist SB203580, or NF‐κB antagonist PDTC did not affect IL‐1β‐evoked tactile allodynia. In conclusion, our data provide additional evidence that RN IL‐1β is involved in pain modulation, and that it exerts a facilitatory effect by activating the JAK/STAT3 and JNK signaling pathways.