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10.1371/journal.pone.0156090 http://scihub22266oqcxt.onion/10.1371/journal.pone.0156090 C4880333!4880333 !27224286     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27224286 &cmd=llinks): Failed to open stream: HTTP request failed! 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Involvement of TGF-?1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice |pdf=|usr=}}{{27224286 }} gab.com Text Involvement of TGF- 1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27224286 #FOAvip Transforming growth factor-beta1 (TGF-?1) is a major factor in pathogenesis of chronic hepatic injury. Carbon tetrachloride (CCl4) is a liver toxicant, and CCl4-induced liver injury in mouse is a classical animal model of chemical liver injury. However, it is still unclear whether TGF-?1 is involved in the process of CCl4-induced acute chemical liver injury. The present study aimed to evaluate the role of TGF-?1 and its signaling molecule Smad3 in the acute liver injury induce by CCl4. The results showed that CCl4 induced acute liver injury in mice effectively confirmed by H&E staining of liver tissues, and levels of not only liver injury markers serum ALT and AST, but also serum TGF-?1 were elevated significantly in CCl4-treated mice, compared with the control mice treated with olive oil. Our data further revealed that TGF-?1 levels in hepatic tissue homogenate increased significantly, and type II receptor of TGF-? (T?RII) and signaling molecules Smad2, 3, mRNA expressions and Smad3 and phospho-Smad3 protein levels also increased obviously in livers of CCl4-treated mice. To clarify the effect of the elevated TGF-?1/Smad3 signaling on CCl4-induced acute liver injury, Smad3 in mouse liver was overexpressed in vivo by tail vein injection of Smad3-expressing plasmids. Upon CCl4 treatment, Smad3-overexpressing mice showed more severe liver injury identified by H&E staining of liver tissues and higher serum ALT and AST levels. Simultaneously, we found that Smad3-overexpressing mice treated with CCl4 showed more macrophages and neutrophils infiltration in liver and inflammatory cytokines IL-1? and IL-6 levels increment in serum when compared with those in control mice treated with CCl4. Moreover, the results showed that the apoptosis of hepatocytes increased significantly, and apoptosis-associated proteins Bax, cytochrome C and the cleaved caspase 3 expressions were up-regulated in CCl4-treated Smad3-overexpressing mice as well. These results suggested that TGF-?1/Smad3 signaling was activated during CCl4-induced acute liver injury in mice, and Smad3 overexpression aggravated acute liver injury by promoting inflammatory cells infiltration, inflammatory cytokines release and hepatocytes apoptosis. In conclusion, the activation of TGF-? signaling contributes to the CCl4-induced acute liver injury. Thus, TGF-?1/Smad3 may serve as a potential target for acute liver injury therapy. Twit Text FOAVip Involvement of TGF- 1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27224286 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27224286 #FOAvip English Wikipedia <ref>{{Cite pmid|27224286 }}</ref> Involvement of TGF-?1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice #MMPMID27224286 Niu L ; Cui X ; Qi Y ; Xie D ; Wu Q ; Chen X ; Ge J ; Liu Z PLoS One 2016[]; 11 (5 ): e0156090 PMID27224286 show ga Transforming growth factor-beta1 (TGF-?1) is a major factor in pathogenesis of chronic hepatic injury. Carbon tetrachloride (CCl4) is a liver toxicant, and CCl4-induced liver injury in mouse is a classical animal model of chemical liver injury. However, it is still unclear whether TGF-?1 is involved in the process of CCl4-induced acute chemical liver injury. The present study aimed to evaluate the role of TGF-?1 and its signaling molecule Smad3 in the acute liver injury induce by CCl4. The results showed that CCl4 induced acute liver injury in mice effectively confirmed by H&E staining of liver tissues, and levels of not only liver injury markers serum ALT and AST, but also serum TGF-?1 were elevated significantly in CCl4-treated mice, compared with the control mice treated with olive oil. Our data further revealed that TGF-?1 levels in hepatic tissue homogenate increased significantly, and type II receptor of TGF-? (T?RII) and signaling molecules Smad2, 3, mRNA expressions and Smad3 and phospho-Smad3 protein levels also increased obviously in livers of CCl4-treated mice. To clarify the effect of the elevated TGF-?1/Smad3 signaling on CCl4-induced acute liver injury, Smad3 in mouse liver was overexpressed in vivo by tail vein injection of Smad3-expressing plasmids. Upon CCl4 treatment, Smad3-overexpressing mice showed more severe liver injury identified by H&E staining of liver tissues and higher serum ALT and AST levels. Simultaneously, we found that Smad3-overexpressing mice treated with CCl4 showed more macrophages and neutrophils infiltration in liver and inflammatory cytokines IL-1? and IL-6 levels increment in serum when compared with those in control mice treated with CCl4. Moreover, the results showed that the apoptosis of hepatocytes increased significantly, and apoptosis-associated proteins Bax, cytochrome C and the cleaved caspase 3 expressions were up-regulated in CCl4-treated Smad3-overexpressing mice as well. These results suggested that TGF-?1/Smad3 signaling was activated during CCl4-induced acute liver injury in mice, and Smad3 overexpression aggravated acute liver injury by promoting inflammatory cells infiltration, inflammatory cytokines release and hepatocytes apoptosis. In conclusion, the activation of TGF-? signaling contributes to the CCl4-induced acute liver injury. Thus, TGF-?1/Smad3 may serve as a potential target for acute liver injury therapy. |Acute Disease [MESH] |Animals [MESH] |Apoptosis/drug effects [MESH] |Carbon Tetrachloride Poisoning/*metabolism/pathology [MESH] |Carbon Tetrachloride/toxicity [MESH] |Chemical and Drug Induced Liver Injury/*metabolism/pathology [MESH] |Hepatocytes/*metabolism/pathology [MESH] |Interleukin-1beta/metabolism [MESH] |Interleukin-6/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Protein Serine-Threonine Kinases/metabolism [MESH] |Receptor, Transforming Growth Factor-beta Type II [MESH] |Receptors, Transforming Growth Factor beta/metabolism [MESH] |Signal Transduction/*drug effects [MESH] |Smad2 Protein/metabolism [MESH] |Smad3 Protein/*metabolism [MESH]Involvement of TGF-?1/Smad3 Signaling in Carbon Tetrachloride-Induced (epmc).pdf DeepDyve Pubget Overpricing