Journal of Cell Communication and Signaling最新文献

{"title":"Transcription factor GTF2I regulates osteoclast differentiation through mediating miR-134-5p and MAT2A expressions","authors":"Lian Tang,&nbsp;Yanshi Liu,&nbsp;Jiyuan Yan,&nbsp;Lin Yuan,&nbsp;Zhaojun Wang,&nbsp;Zhong Li","doi":"10.1002/ccs3.70010","DOIUrl":"https://doi.org/10.1002/ccs3.70010","url":null,"abstract":"<p>This study explored the possible effect of transcription factor GTF2I on the differentiation of osteoclasts and its regulation on the miR-134-5p/MAT2A axis. RANKL-induced osteoclasts were measured for expressions of GTF2I, miR-134-5p, and MAT2A. The number and size of osteoclasts were assessed after TRAP staining. The expressions of osteoclast differentiation biomarkers, NFATC1, TRAP, and CTSK, were detected as well. The relationships of the GTF2I/miR-134-5p/MAT2A axis were verified by ChIP, dual luciferase, and RNA pull-down assay. In vivo experiments were conducted on ovariectomized (OVX)-treated mice to determine the effect of GTF2I overexpression on osteoclast differentiation and bone loss. RANKL-induced osteoclasts had suppressed expressions of GTF2I and miR-134-5p and increased expression of MAT2A. GTF2I overexpression or miR-134-5p overexpression contributed to decreased cell number and size and suppressed cell differentiation, whereas such an effect can be abolished by overexpression of MAT2A. GTF2I can bind the miR-134-5p promoter to regulate its expression, whereas miR-134-5p can negatively regulate MAT2A expression. The protective effect of GTF2I overexpression against bone loss and cell differentiation was verified by in vivo experiments. Collectively, these results indicate that GTF2I can mediate miR-134-5p expression to increase MAT2A expression, contributing to the suppression of osteoclast differentiation.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143770359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of altered cell–cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points","authors":"Tabea M. Soelter,&nbsp;Timothy C. Howton,&nbsp;Elizabeth J. Wilk,&nbsp;Jordan H. Whitlock,&nbsp;Amanda D. Clark,&nbsp;Allison Birnbaum,&nbsp;Dalton C. Patterson,&nbsp;Constanza J. Cortes,&nbsp;Brittany N. Lasseigne","doi":"10.1002/ccs3.70006","DOIUrl":"https://doi.org/10.1002/ccs3.70006","url":null,"abstract":"<p>Alzheimer's disease (AD) is the most common form of dementia and is characterized by progressive memory loss and cognitive decline, affecting behavior, speech, and motor abilities. The neuropathology of AD includes the formation of extracellular amyloid-β plaques and intracellular neurofibrillary tangles of phosphorylated tau, along with neuronal loss. Although neuronal loss is an AD hallmark, cell–cell communication between neuronal and non-neuronal cell populations maintains neuronal health and brain homeostasis. To study changes in cell–cell communication during disease progression, we performed snRNA-sequencing of the hippocampus from female 3xTg-AD and wild-type littermates at 6 and 12 months. We inferred differential cell–cell communication between 3xTg-AD and wild-type mice across time points and between senders (astrocytes, microglia, oligodendrocytes, and OPCs) and receivers (excitatory and inhibitory neurons) of interest. We also assessed the downstream effects of altered glia–neuron communication using pseudobulk differential gene expression, functional enrichment, and gene regulatory analyses. We found that glia–neuron communication is increasingly dysregulated in 12-month 3xTg-AD mice. We also identified 23 AD-associated ligand–receptor pairs that are upregulated in the 12-month-old 3xTg-AD hippocampus. Our results suggest increased AD association of interactions originating from microglia. Signaling mediators were not significantly differentially expressed but showed altered gene regulation and transcription factor activity. Our findings indicate that altered glia–neuron communication is increasingly dysregulated and affects the gene regulatory mechanisms in neurons of 12-month-old 3xTg-AD mice.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143521842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0000515 sequesters microRNA-296-5p and elevates RNF44 expression to encourage the NSCLC progression","authors":"Lixin Sun,&nbsp;Bei Lu,&nbsp;Chongyuan Li,&nbsp;Guangquan Xu","doi":"10.1002/ccs3.70005","DOIUrl":"https://doi.org/10.1002/ccs3.70005","url":null,"abstract":"<p>Circular RNAs (circRNAs) are RNA molecules frequently involved in tumorigenesis. This research study focuses on the relevance of hsa_circ_515 (circ_515) to non-small cell lung cancer (NSCLC) progression and the downstream targets involved. Differentially expressed circRNAs in NSCLC were screened using a GSE158695 dataset. Circ_515 was overexpressed and indicated poor outcomes in patients with NSCLC. Knockdown of circ_515 repressed proliferation and invasiveness, while potentiated cell cycle arrest and apoptosis of NSCLC cells, and upregulation of circ_515 led to converse trends. The candidate downstream transcripts of circ_515 were explored using integrated bioinformatic analyses. Ectopic expression of miR-296-5p reduced the malignance of NSCLC cells. Circ_515 sequestered miR-296-5p and blocked its suppressive role in RING finger protein 44 (RNF44) expression. Downregulation of RNF44 counteracted the oncogenic effects of circ_515. In vivo, the anti-tumor effects of circ_515 knockdown were reversed by miR-296-5p, while the tumor-promoting effects of circ_515 upregulation were abolished by RNF44 knockdown. All in all, our findings demonstrate that circ_515 sequesters miR-296-5p and elevates RNF44 expression to encourage the NSCLC progression. This study might provide new thoughts on NSCLC management.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moscatilin alleviates oxidative stress and inflammatory response of Müller cells in diabetic retinopathy through suppressing the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase and nuclear factor kappa-B signaling pathways","authors":"Suhua Zhu,&nbsp;Man Zhang,&nbsp;Zhen Qu,&nbsp;Shengqiu Xu,&nbsp;Jie Peng,&nbsp;Fanjing Jiang","doi":"10.1002/ccs3.12059","DOIUrl":"https://doi.org/10.1002/ccs3.12059","url":null,"abstract":"<p>Diabetic retinopathy (DR), as the main ophthalmic complication of diabetes mellitus, is a major eye disorder contributing to blindness. Oxidative stress and inflammation in retinal Müller cells participate in the pathogenesis of DR. This work aims to study the biological role of moscatilin in the progression of DR and the underlying mechanism. High glucose (HG)-stimulated mouse primary retinal Müller cells and high-fat diet + streptozotocin (STZ)-induced DR mouse models were constructed as in vitro and in vivo models, respectively. The effects of moscatilin treatment on oxidative stress and inflammation in HG-stimulated Müller cells and DR mice were evaluated by detecting intracellular reactive oxygen species production, malondialdehyde levels, superoxide dismutase and catalase activities, glutathione/oxidized glutathione ratio, as well as proinflammatory cytokine levels through CM-H₂DCFDA staining, commercial kits, and enzyme-linked immunosorbent assay. Dual immunofluorescence staining of glial fibrillary acidic protein and vimentin was used to evaluate the development of Müller cells in mouse retinas. The activity of p38 mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinase (JNK) and nuclear factor kappa-B (NF-κB) signaling pathway was assessed through western blotting and immunofluorescence staining. Moscatilin pretreatment prevented HG-induced decrease in Müller cell viability. Moscatilin mitigated oxidative stress, inflammation, and extracellular matrix remodeling in HG-stimulated Müller cells and DR mice. Mechanically, moscatilin reduced the levels of receptor for advanced glycation end products, phosphorylated I-kappa-B-alpha, p-p65 NF-κB, p-p38 MAPK, and p-JNK in both HG-stimulated Müller cells and DR mice. Moscatilin plays an antioxidant and anti-inflammatory role in DR by inhibiting the p38 MAPK/JNK and NF-κB signaling pathways.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143446958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stepping into the role of Editor-in-Chief of the Journal of Cell Communication and Signaling","authors":"Brahim Chaqour","doi":"10.1002/ccs3.70000","DOIUrl":"https://doi.org/10.1002/ccs3.70000","url":null,"abstract":"<p>I am deeply honored to have been appointed as the new Editor-in-Chief (EiC) of the <i>Journal of Cell Communication and Signaling</i> (<i>JCCS</i>). As I step into this role of EiC, I look forward to continuing collaborating with the dedicated readership, expert reviewers, editorial board members, and the publisher of the journal to advancing knowledge in research on cell communication and signaling governing key biochemical and physiological processes both in normal and pathological conditions. <i>JCCS</i> remains dedicated to publishing cutting-edge research, while continuously expanding the range of submissions and refining the review and editorial processes to ensure a more inclusive and impactful scientific contribution. I would like to thank the founder of <i>JCCS</i> and my predecessor EiC, Prof. Bernard Perbal and his right hand Annick Perbal for their enormous contribution to <i>JCCS</i>, and their crucial role shaping the Journal into a platform that welcomes innovative research and enhances our understanding of cellular communication networks in health and diseases and for steering us safely over the last two decades through the increasingly challenging scientific publication landscape. In this editorial, I share some of my reflections, ideas, acknowledgments, and aspirations for the future of the journal.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70000","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143404425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the calcium-sensing receptor in regulating vascular function","authors":"Anthony P. Albert,&nbsp;Harry Z.E. Greenberg","doi":"10.1002/ccs3.70004","DOIUrl":"https://doi.org/10.1002/ccs3.70004","url":null,"abstract":"<p>Functional expression of the calcium-sensing receptor (CaSR) in calcitropic tissues, for example, parathyroid glands and kidneys, is important for maintaining Ca²⁺ homeostasis. It is also established that the CaSR is present in tissues previously thought to be noncalcitropic and this review discusses the role of the CaSR in vascular function, focusing mainly on contractility but also outlining its role in cell proliferation and calcification. Stimulation of the CaSR by extracellular Ca²⁺ concentration ([Ca²⁺]_o) on perivascular sensory nerves and vascular endothelial cells is associated with vasodilatation through the release of vasoactive substances and stimulation of IK_Ca channels and nitric oxide synthesis, respectively, which mediate endothelium-derived hyperpolarizations and activation of BK_Ca channels and K_ATP channels in vascular smooth muscle cells (VSMCs). CaSR-induced vasoconstrictions are mediated by the CaSR expressed in VSMCs, which are coupled to the G_q/11 protein-coupled pathway. In addition, the CaSR expressed on VSMCs also regulates proliferation and calcification. Consequently, the CaSR has been implicated in regulating systemic and pulmonary blood pressure and calcimimetics and calcilytics are potential therapeutic targets for cardiovascular diseases, such as hypertension, pulmonary artery hypertension, and atherosclerosis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143248753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCN2 functions as a modulator of cell cycle regulation in human dermal fibroblasts","authors":"Taihao Quan,&nbsp;Yuan Shao,&nbsp;Trupta Purohit,&nbsp;Yiou Jiang,&nbsp;Zhaoping Qin,&nbsp;Gary J. Fisher,&nbsp;Nathan H. Lents,&nbsp;Joseph J. Baldassare","doi":"10.1002/ccs3.70003","DOIUrl":"10.1002/ccs3.70003","url":null,"abstract":"<p>CCN2 is widely regarded as a profibrotic factor involved in fibrotic disorders by regulating extracellular matrix (ECM). We report here that CCN2 functions as a critical cell cycle regulator in primary human dermal fibroblasts (HDFs). siRNA-mediated knockdown of CCN2 halted proliferation of primary HDFs, which was rescued by a siRNA-resistant CCN2 expression vector. Furthermore, CCN2 knockdown caused a significant accumulation of cells in G1/G0 phase and blocked entry into S-phase. Mechanistically, CCN2 knockdown blocked cyclin E and CDK4/cyclin D nuclear translocation, and abrogated CDK2 activity. Markedly, CCN2 translocated to the nucleus and co-localized with cyclin D1 upon cell cycle stimulation. Finally, we show that CCN2, a bona fide YAP/TAZ target gene, partially mediates YAP/TAZ-dependent proliferation of primary HDFs. These data provide evidence of a novel CCN2 function as a cell cycle regulator in primary HDFs proliferation, in addition to its known role in ECM regulation.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The opposite effect of ELP4 and ZEB2 on TCF7L2-mediated microglia polarization in ischemic stroke","authors":"Xiao-li Min,&nbsp;Sixian Lin,&nbsp;Jia-yi Hu,&nbsp;Rui Jing,&nbsp;Qing Zhao,&nbsp;Fei-fei Shang,&nbsp;Yong Zeng","doi":"10.1002/ccs3.12061","DOIUrl":"10.1002/ccs3.12061","url":null,"abstract":"<p>Microglia M1 polarization plays important role in the development of ischemic stroke (IS). This study explored the role of transcription factor 7 like 2 (TCF7L2) in regulating microglia M1 polarization during IS. TTC staining was used to determine the cerebral infarction, and Nissl staining was applied to examine neuronal injury. The secretion levels of cytokines were measured using ELISA. The interaction between Zinc finger E-Box binding homeobox 2 (ZEB2) and TCF7L2 was analyzed by Co-IP, and H3K27ac enrichment in the TCF7L2 promoter was detected by ChIP assay. TCF7L2 knockdown reduced MCAO/R-induced mice cerebral injury. TCF7L2 silencing or TAK-242 (TLR4 antagonist) injection inhibited OGD/R-induced microglia M1 polarization by repressing the TLR4/NF-κB signal, and TCF7L2 knockdown combined with TAK-242 treatment further inhibited microglia M1 polarization. TCF7L2 promoted transcriptional activation of TLR4. ELP4 enhanced H3K27ac-mediated transcriptional activation of TCF7L2, and ZEB2 promoted the K48-linked ubiquitination of TCF7L2. TCF7L2 overexpression abolished the inhibitory effect of ELP4 knockdown or ZEB2 overexpression on OGD/R-induced microglia M1 polarization. TCF7L2 exacerbated cerebral injury by promoting microglia M1 polarization during IS progression. Mechanistically, ELP4 promoted TCF7L2 expression by promoting H3K27ac enrichment in the TCF7L2 promoter, while ZEB2 promoted TCF7L2 ubiquitination degradation.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"I had a dream","authors":"Bernard Perbal","doi":"10.1002/ccs3.12064","DOIUrl":"10.1002/ccs3.12064","url":null,"abstract":"<p>Expressing hopes and desires is an essential part of communication, and communication is the major pillar of the Journal of Cell Communication and Signaling. There comes the time of giving the responsibility of leading JCCS to a new editor in chief and I am taking this opportunity to comment on a few recent milestones and future of the journal which I created in 2007, after I had created “Cell Communication and Signaling” 20 years ago (1), one of the first open access journals.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11727572/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"M2-polarized tumor-associated macrophage-secreted exosomal lncRNA NEAT1 upregulates galectin-3 by recruiting KLF5 and promotes HCC immune escape","authors":"Wei Yuan,&nbsp;Qigang Sun,&nbsp;Xiaodan Zhu,&nbsp;Bo Li,&nbsp;Yongping Zou,&nbsp;Zhehao Liu","doi":"10.1002/ccs3.12060","DOIUrl":"10.1002/ccs3.12060","url":null,"abstract":"<p>HCC cell immune escape is a critical element in the evolution of HCC malignancy. Herein, the regulatory mechanism of lncRNA NEAT1 in regulating HCC immune escape was investigated. Exosomes were isolated from M2 TAMs using ExoQuick-TC. Then, HCC cells were incubated with M2 TAMs-derived exosomes (M2-exos). The activation of perforin⁺CD8⁺ T cells was measured using flow cytometry. The secretion of IFN-γ was assessed using ELISA. Cell viability and migration were detected using CCK8 and Transwell assays, respectively. RIP and RNA pull-down assays were used to investigate the link between NEAT1 and KLF5. ChIP and dual-luciferase reporter assays were used to investigate the interaction between KLF5 and the LGALS3 promoter. Our results showed that NEAT1, KLF5 and galectin-3 were overexpressed in HCC tissues. M2-exos treatment promoted HCC proliferation, migration, and immune escape. It was found that NEAT1 was enriched in M2-TAMs and M2-exos. M2-exos facilitated HCC immune escape, whereas NEAT1 silencing reversed this effect. NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5. Mechanically, M2-TAM-derived exosomal NEAT1 induced HCC immune escape by upregulating KLF5/galectin-3 axis. M2-TAM-derived exosomal NEAT1 upregulated galectin-3 in HCC cells by recruiting KLF5 to promote perforin⁺CD8⁺ T cell depletion and further accelerate HCC immune escape.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11666343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}