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10.1186/s13287-016-0424-y http://scihub22266oqcxt.onion/10.1186/s13287-016-0424-y C5120504!5120504 !27876093     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27876093 &cmd=llinks): Failed to open stream: HTTP request failed! 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Involvement of hepatic macrophages in the antifibrotic effect of IGF-I-overexpressing mesenchymal stromal cells |pdf=|usr=}}{{27876093 }} gab.com Text Involvement of hepatic macrophages in the antifibrotic effect of IGF-I-overexpressing mesenchymal stromal cells JO: Stem Cell Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=27876093 #FOAvip BACKGROUND: Cirrhosis is a major health problem worldwide and new therapies are needed. Hepatic macrophages (hMų) have a pivotal role in liver fibrosis, being able to act in both its promotion and its resolution. It is well-known that mesenchymal stromal cells (MSCs) can modulate the immune/inflammatory cells. However, the effects of MSCs over hMų in the context of liver fibrosis remain unclear. We previously described evidence of the antifibrotic effects of in vivo applying MSCs, which were enhanced by forced overexpression of insulin-like growth factor 1 (AdIGF-I-MSCs). The aim of this work was to analyze the effect of MSCs on hMų behavior in the context of liver fibrosis resolution. METHODS: Fibrosis was induced in BALB/c mice by chronic administration of thioacetamide (8 weeks). In vivo gene expression analyses, in vitro experiments using hMų isolated from the nonparenchymal liver cells fraction, and in vivo experiments with depletion of Mų were performed. RESULTS: One day after treatment, hMų from fibrotic livers of MSCs-treated animals showed reduced pro-inflammatory and pro-fibrogenic gene expression profiles. These shifts were more pronounced in AdIGF-I-MSCs condition. This group showed a significant upregulation in the expression of arginase-1 and a higher downregulation of iNOS expression thus suggesting decreased levels of oxidative stress. An upregulation in IGF-I and HGF expression was observed in hMų from AdIGF-I-MSCs-treated mice suggesting a restorative phenotype in these cells. Factors secreted by hMų, preconditioned with MSCs supernatant, caused a reduction in the expression levels of hepatic stellate cells pro-fibrogenic and activation markers. Interestingly, hMų depletion abrogated the therapeutic effect achieved with AdIGF-I-MSCs therapy. Expression profile analyses for cell cycle markers were performed on fibrotic livers after treatment with AdIGF-I-MSCs and showed a significant regulation in genes related to DNA synthesis and repair quality control, cell cycle progression, and DNA damage/cellular stress compatible with early induction of pro-regenerative and hepatoprotective mechanisms. Moreover, depletion of hMų abrogated such effects on the expression of the most highly regulated genes. CONCLUSIONS: Our results indicate that AdIGF-I-MSCs are able to induce a pro-fibrotic to resolutive phenotype shift on hepatic macrophages, which is a key early event driving liver fibrosis amelioration. Twit Text FOAVip Involvement of hepatic macrophages in the antifibrotic effect of IGF-I-overexpressing mesenchymal stromal cells ????Stem Cell Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=27876093 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27876093 #FOAvip English Wikipedia <ref>{{Cite pmid|27876093 }}</ref> Involvement of hepatic macrophages in the antifibrotic effect of IGF-I-overexpressing mesenchymal stromal cells #MMPMID27876093 Fiore E ; Malvicini M ; Bayo J ; Peixoto E ; Atorrasagasti C ; Sierra R ; Rodrķguez M ; Gómez Bustillo S ; Garcķa MG ; Aquino JB ; Mazzolini G Stem Cell Res Ther 2016[Nov]; 7 (1 ): 172 PMID27876093 show ga BACKGROUND: Cirrhosis is a major health problem worldwide and new therapies are needed. Hepatic macrophages (hMų) have a pivotal role in liver fibrosis, being able to act in both its promotion and its resolution. It is well-known that mesenchymal stromal cells (MSCs) can modulate the immune/inflammatory cells. However, the effects of MSCs over hMų in the context of liver fibrosis remain unclear. We previously described evidence of the antifibrotic effects of in vivo applying MSCs, which were enhanced by forced overexpression of insulin-like growth factor 1 (AdIGF-I-MSCs). The aim of this work was to analyze the effect of MSCs on hMų behavior in the context of liver fibrosis resolution. METHODS: Fibrosis was induced in BALB/c mice by chronic administration of thioacetamide (8 weeks). In vivo gene expression analyses, in vitro experiments using hMų isolated from the nonparenchymal liver cells fraction, and in vivo experiments with depletion of Mų were performed. RESULTS: One day after treatment, hMų from fibrotic livers of MSCs-treated animals showed reduced pro-inflammatory and pro-fibrogenic gene expression profiles. These shifts were more pronounced in AdIGF-I-MSCs condition. This group showed a significant upregulation in the expression of arginase-1 and a higher downregulation of iNOS expression thus suggesting decreased levels of oxidative stress. An upregulation in IGF-I and HGF expression was observed in hMų from AdIGF-I-MSCs-treated mice suggesting a restorative phenotype in these cells. Factors secreted by hMų, preconditioned with MSCs supernatant, caused a reduction in the expression levels of hepatic stellate cells pro-fibrogenic and activation markers. Interestingly, hMų depletion abrogated the therapeutic effect achieved with AdIGF-I-MSCs therapy. Expression profile analyses for cell cycle markers were performed on fibrotic livers after treatment with AdIGF-I-MSCs and showed a significant regulation in genes related to DNA synthesis and repair quality control, cell cycle progression, and DNA damage/cellular stress compatible with early induction of pro-regenerative and hepatoprotective mechanisms. Moreover, depletion of hMų abrogated such effects on the expression of the most highly regulated genes. CONCLUSIONS: Our results indicate that AdIGF-I-MSCs are able to induce a pro-fibrotic to resolutive phenotype shift on hepatic macrophages, which is a key early event driving liver fibrosis amelioration. |Animals [MESH] |Cells, Cultured [MESH] |Down-Regulation/drug effects [MESH] |Gene Expression/drug effects [MESH] |Hepatic Stellate Cells/drug effects/metabolism/physiology [MESH] |Hepatocyte Growth Factor/metabolism [MESH] |Hepatocytes/drug effects/metabolism [MESH] |Insulin-Like Growth Factor I/*metabolism [MESH] |Liver Cirrhosis/metabolism/*therapy [MESH] |Liver/drug effects/metabolism [MESH] |Macrophages/*cytology/drug effects/metabolism [MESH] |Male [MESH] |Mesenchymal Stem Cells/*cytology/*metabolism [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Thioacetamide/pharmacology [MESH]Involvement of hepatic macrophages in the antifibrotic effect of IGF(epmc).pdf DeepDyve Pubget Overpricing