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10.1172/jci.insight.97732 http://scihub22266oqcxt.onion/10.1172/jci.insight.97732 C5821176!5821176 !29415896     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29415896 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29415896 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       JCI+Insight 2018 ; 3 (3 ): ä Nephropedia Template TP {{tp|p=29415896 |t=2018. Virus-like infection induces human ? cell dedifferentiation |pdf=|usr=}}{{29415896 }} gab.com Text Virus-like infection induces human cell dedifferentiation JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29415896 #FOAvip Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic ? cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than ? cell death, suggesting loss of ? cell identity. We undertook this study to examine whether viral infection could induce human ? cell dedifferentiation. Using the functional human ? cell line EndoC-?H1, we demonstrate that polyinosinic-polycytidylic acid (PolyI:C), a synthetic double-stranded RNA that mimics a byproduct of viral replication, induces a decrease in ? cell-specific gene expression. In parallel with this loss, the expression of progenitor-like genes such as SOX9 was activated following PolyI:C treatment or enteroviral infection. SOX9 was induced by the NF-?B pathway and also in a paracrine non-cell-autonomous fashion through the secretion of IFN-?. Lastly, we identified SOX9 targets in human ? cells as potentially new markers of dedifferentiation in T1D. These findings reveal that inflammatory signaling has clear implications in human ? cell dedifferentiation. Twit Text FOAVip Virus-like infection induces human cell dedifferentiation ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29415896 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29415896 #FOAvip English Wikipedia <ref>{{Cite pmid|29415896 }}</ref> Virus-like infection induces human ? cell dedifferentiation #MMPMID29415896 Oshima M ; Knoch KP ; Diedisheim M ; Petzold A ; Cattan P ; Bugliani M ; Marchetti P ; Choudhary P ; Huang GC ; Bornstein SR ; Solimena M ; Albagli-Curiel O ; Scharfmann R JCI Insight 2018[Feb]; 3 (3 ): ä PMID29415896 show ga Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic ? cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than ? cell death, suggesting loss of ? cell identity. We undertook this study to examine whether viral infection could induce human ? cell dedifferentiation. Using the functional human ? cell line EndoC-?H1, we demonstrate that polyinosinic-polycytidylic acid (PolyI:C), a synthetic double-stranded RNA that mimics a byproduct of viral replication, induces a decrease in ? cell-specific gene expression. In parallel with this loss, the expression of progenitor-like genes such as SOX9 was activated following PolyI:C treatment or enteroviral infection. SOX9 was induced by the NF-?B pathway and also in a paracrine non-cell-autonomous fashion through the secretion of IFN-?. Lastly, we identified SOX9 targets in human ? cells as potentially new markers of dedifferentiation in T1D. These findings reveal that inflammatory signaling has clear implications in human ? cell dedifferentiation. |Cell Dedifferentiation/drug effects/*immunology [MESH] |Cell Line [MESH] |Diabetes Mellitus, Type 1/*immunology/virology [MESH] |Enterovirus Infections/*immunology/virology [MESH] |Enterovirus/immunology [MESH] |Gene Expression Profiling [MESH] |Gene Expression Regulation/drug effects/immunology [MESH] |Humans [MESH] |Insulin-Secreting Cells/*physiology [MESH] |Interferon Inducers/pharmacology [MESH] |Interferon-alpha/immunology/metabolism [MESH] |NF-kappa B/metabolism [MESH] |Poly I-C/pharmacology [MESH] |Primary Cell Culture [MESH] |SOX9 Transcription Factor/metabolism [MESH]Virus-like infection induces human ? cell dedifferentiation (epmc).pdf DeepDyve Pubget Overpricing