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10.1038/cddis.2014.257 http://scihub22266oqcxt.onion/10.1038/cddis.2014.257 C4611730!4611730 !24967970     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24967970 &cmd=llinks): Failed to open stream: HTTP request failed! 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Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF-?1 generation |pdf=|usr=}}{{24967970 }} gab.com Text Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF- 1 generation JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24967970 #FOAvip Chronic psychological stress has been demonstrated to play an important role in several severe diseases, but whether it affects disease therapy or not remains unclear. Mesenchymal stem cells (MSCs) have been demonstrated to have therapeutic potentials in treating tissue injury based on their multidifferentiation potential toward various cell types. We investigated the effect of chronic restraint stress on therapeutic potential of MSCs on carbon tetrachloride (CCl4)-induced liver injury in mice. CCl4-induced mice were injected with enhanced green fluorescent protein-MSCs, which was followed by chronic restraint stress administration. Corticosterone and RU486, a glucocorticoid receptor (GR) antagonist, were employed in vivo and in vitro, too. In the present study, we illustrated that MSCs could repair liver injury by differentiating into myofibroblasts (MFs) which contribute to fibrosis, whereas stress repressed differentiation of MSCs into MFs displayed by reducing ?-smooth muscle actin (?-SMA, a solid marker of MFs) expression. Whereas RU486 could maintain the liver injury reduction and liver fibrosis increases induced by MSCs in stressed mice and block the decrease of ?-SMA expression induced by stress. Furthermore, chronic stress inhibited MFs differentiation from MSCs by inhibiting transforming growth factor-?1 (TGF-?1)/Smads signaling pathway which is essential for MFs differentiation. Chronic stress reduced autocrine TGF-?1 of MSCs, but not blunted activation of Smads. All these data suggested that corticosterone triggered by chronic stress impaired liver injury repair by MSCs through inhibiting TGF-?1 expression which results in reduced MFs differentiation of MSCs. Twit Text FOAVip Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF- 1 generation ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=24967970 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24967970 #FOAvip English Wikipedia <ref>{{Cite pmid|24967970 }}</ref> Chronic restraint stress decreases the repair potential from mesenchymal stem cells on liver injury by inhibiting TGF-?1 generation #MMPMID24967970 Yang X ; Han ZP ; Zhang SS ; Zhu PX ; Hao C ; Fan TT ; Yang Y ; Li L ; Shi YF ; Wei LX Cell Death Dis 2014[Jun]; 5 (6 ): e1308 PMID24967970 show ga Chronic psychological stress has been demonstrated to play an important role in several severe diseases, but whether it affects disease therapy or not remains unclear. Mesenchymal stem cells (MSCs) have been demonstrated to have therapeutic potentials in treating tissue injury based on their multidifferentiation potential toward various cell types. We investigated the effect of chronic restraint stress on therapeutic potential of MSCs on carbon tetrachloride (CCl4)-induced liver injury in mice. CCl4-induced mice were injected with enhanced green fluorescent protein-MSCs, which was followed by chronic restraint stress administration. Corticosterone and RU486, a glucocorticoid receptor (GR) antagonist, were employed in vivo and in vitro, too. In the present study, we illustrated that MSCs could repair liver injury by differentiating into myofibroblasts (MFs) which contribute to fibrosis, whereas stress repressed differentiation of MSCs into MFs displayed by reducing ?-smooth muscle actin (?-SMA, a solid marker of MFs) expression. Whereas RU486 could maintain the liver injury reduction and liver fibrosis increases induced by MSCs in stressed mice and block the decrease of ?-SMA expression induced by stress. Furthermore, chronic stress inhibited MFs differentiation from MSCs by inhibiting transforming growth factor-?1 (TGF-?1)/Smads signaling pathway which is essential for MFs differentiation. Chronic stress reduced autocrine TGF-?1 of MSCs, but not blunted activation of Smads. All these data suggested that corticosterone triggered by chronic stress impaired liver injury repair by MSCs through inhibiting TGF-?1 expression which results in reduced MFs differentiation of MSCs. |*Mesenchymal Stem Cell Transplantation [MESH] |*Stress, Physiological [MESH] |Allografts [MESH] |Animals [MESH] |Anti-Inflammatory Agents/pharmacology [MESH] |Carbon Tetrachloride Poisoning/genetics/metabolism/pathology/*therapy [MESH] |Cell Differentiation/drug effects/genetics [MESH] |Chemical and Drug Induced Liver Injury/genetics/metabolism/pathology/*therapy [MESH] |Chronic Disease [MESH] |Corticosterone/metabolism/pharmacology [MESH] |Gene Expression Regulation/drug effects/genetics [MESH] |Hormone Antagonists/pharmacology [MESH] |Liver Cirrhosis/genetics/metabolism/pathology/therapy [MESH] |Male [MESH] |Mesenchymal Stem Cells/*metabolism/pathology [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Mifepristone/pharmacology [MESH] |Restraint, Physical [MESH] |Signal Transduction/drug effects/genetics [MESH] |Smad Proteins/genetics/metabolism [MESH]Chronic restraint stress decreases the repair potential from mesenchym(epmc).pdf DeepDyve Pubget Overpricing