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10.1038/s41419-017-0071-y http://scihub22266oqcxt.onion/10.1038/s41419-017-0071-y C5833779!5833779 !29352207     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 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\29352207 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Death+Dis 2018 ; 9 (2 ): 51 Nephropedia Template TP {{tp|p=29352207 |t=2018. Ethanol sensitizes hepatocytes for TGF-?-triggered apoptosis |pdf=|usr=}}{{29352207 }} gab.com Text Ethanol sensitizes hepatocytes for TGF- -triggered apoptosis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29352207 #FOAvip Alcohol abuse is a global health problem causing a substantial fraction of chronic liver diseases. Abundant TGF-?-a potent pro-fibrogenic cytokine-leads to disease progression. Our aim was to elucidate the crosstalk of TGF-? and alcohol on hepatocytes. Primary murine hepatocytes were challenged with ethanol and TGF-? and cell fate was determined. Fluidigm RNA analyses revealed transcriptional effects that regulate survival and apoptosis. Mechanistic insights were derived from enzyme/pathway inhibition experiments and modulation of oxidative stress levels. To substantiate findings, animal model specimens and human liver tissue cultures were investigated. RESULTS: On its own, ethanol had no effect on hepatocyte apoptosis, whereas TGF-? increased cell death. Combined treatment led to massive hepatocyte apoptosis, which could also be recapitulated in human HCC liver tissue treated ex vivo. Alcohol boosted the TGF-? pro-apoptotic gene signature. The underlying mechanism of pathway crosstalk involves SMAD and non-SMAD/AKT signaling. Blunting CYP2E1 and ADH activities did not prevent this effect, implying that it was not a consequence of alcohol metabolism. In line with this, the ethanol metabolite acetaldehyde did not mimic the effect and glutathione supplementation did not prevent the super-induction of cell death. In contrast, blocking GSK-3? activity, a downstream mediator of AKT signaling, rescued the strong apoptotic response triggered by ethanol and TGF-?. This study provides novel information on the crosstalk between ethanol and TGF-?. We give evidence that ethanol directly leads to a boost of TGF-?'s pro-apoptotic function in hepatocytes, which may have implications for patients with chronic alcoholic liver disease. Twit Text FOAVip Ethanol sensitizes hepatocytes for TGF- -triggered apoptosis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29352207 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29352207 #FOAvip English Wikipedia <ref>{{Cite pmid|29352207 }}</ref> Ethanol sensitizes hepatocytes for TGF-?-triggered apoptosis #MMPMID29352207 Gaitantzi H ; Meyer C ; Rakoczy P ; Thomas M ; Wahl K ; Wandrer F ; Bantel H ; Alborzinia H ; Wölfl S ; Ehnert S ; Nüssler A ; Bergheim I ; Ciuclan L ; Ebert M ; Breitkopf-Heinlein K ; Dooley S Cell Death Dis 2018[Jan]; 9 (2 ): 51 PMID29352207 show ga Alcohol abuse is a global health problem causing a substantial fraction of chronic liver diseases. Abundant TGF-?-a potent pro-fibrogenic cytokine-leads to disease progression. Our aim was to elucidate the crosstalk of TGF-? and alcohol on hepatocytes. Primary murine hepatocytes were challenged with ethanol and TGF-? and cell fate was determined. Fluidigm RNA analyses revealed transcriptional effects that regulate survival and apoptosis. Mechanistic insights were derived from enzyme/pathway inhibition experiments and modulation of oxidative stress levels. To substantiate findings, animal model specimens and human liver tissue cultures were investigated. RESULTS: On its own, ethanol had no effect on hepatocyte apoptosis, whereas TGF-? increased cell death. Combined treatment led to massive hepatocyte apoptosis, which could also be recapitulated in human HCC liver tissue treated ex vivo. Alcohol boosted the TGF-? pro-apoptotic gene signature. The underlying mechanism of pathway crosstalk involves SMAD and non-SMAD/AKT signaling. Blunting CYP2E1 and ADH activities did not prevent this effect, implying that it was not a consequence of alcohol metabolism. In line with this, the ethanol metabolite acetaldehyde did not mimic the effect and glutathione supplementation did not prevent the super-induction of cell death. In contrast, blocking GSK-3? activity, a downstream mediator of AKT signaling, rescued the strong apoptotic response triggered by ethanol and TGF-?. This study provides novel information on the crosstalk between ethanol and TGF-?. We give evidence that ethanol directly leads to a boost of TGF-?'s pro-apoptotic function in hepatocytes, which may have implications for patients with chronic alcoholic liver disease. |Animals [MESH] |Apoptosis [MESH] |Ethanol/*adverse effects [MESH] |Hepatocytes/*metabolism [MESH] |Humans [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH]Ethanol sensitizes hepatocytes for TGF-?-triggered apoptosis (epmc).pdf DeepDyve Pubget Overpricing