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10.1186/s12967-018-1493-8 http://scihub22266oqcxt.onion/10.1186/s12967-018-1493-8 C5935959!5935959 !29728112     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29728112 &cmd=llinks): Failed to open stream: HTTP request failed! 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Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury |pdf=|usr=}}{{29728112 }} gab.com Text Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury JO: J Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=29728112 #FOAvip BACKGROUND: Ischemia-reperfusion (I/R)-induced acute kidney injury (AKI) not only prolongs the length of hospital stay, but also seriously affects the patient's survival rate. Although our previous investigation has verified that reactive oxygen species (ROS) transferred through gap junction composed of connexin32 (Cx32) contributed to AKI, its underlying mechanisms were not fully understood and viable preventive or therapeutic regimens were still lacking. Among various mechanisms involved in organs I/R-induced injuries, endoplasmic reticulum stress (ERS)-related apoptosis is currently considered to be an important participant. Thus, in present study, we focused on the underlying mechanisms of I/R-induced AKI, and postulated that Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. METHODS: We established renal I/R models with Cx32(+/+) and Cx32(-/-) mice, which underwent double kidneys clamping and recanalization. ROS scavenger (N-acetylcysteine, NAC) and ERS inhibitors (4-phenyl butyric acid, 4-PBA, and tauroursodeoxycholic acid, TUDCA) were used to decrease the content of ROS and attenuate ERS activation, respectively. RESULTS: Renal damage was progressively exacerbated in a time-dependent manner at the reperfusion stage, that was consistent with the alternation of ERS activation, including glucose regulated protein 78 (BiP/GRP78), X box-binding protein1, and C/EBP homologous protein expression. TUDCA or 4-PBA application attenuated I/R-induced ERS activation and protected against renal tubular epithelial cells apoptosis and renal damage. Cx32 deficiency decreased ROS generation and distribution between the neighboring cells, which attenuated I/R-induced ERS activation, and improved cell apoptosis and renal damage. CONCLUSION: Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Cx32 deficiency, ROS elimination, and ERS inhibition all could protect against I/R-induced AKI. Twit Text FOAVip Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury ????J Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=29728112 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29728112 #FOAvip English Wikipedia <ref>{{Cite pmid|29728112 }}</ref> Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury #MMPMID29728112 Gu Y ; Huang F ; Wang Y ; Chen C ; Wu S ; Zhou S ; Hei Z ; Yuan D J Transl Med 2018[May]; 16 (1 ): 117 PMID29728112 show ga BACKGROUND: Ischemia-reperfusion (I/R)-induced acute kidney injury (AKI) not only prolongs the length of hospital stay, but also seriously affects the patient's survival rate. Although our previous investigation has verified that reactive oxygen species (ROS) transferred through gap junction composed of connexin32 (Cx32) contributed to AKI, its underlying mechanisms were not fully understood and viable preventive or therapeutic regimens were still lacking. Among various mechanisms involved in organs I/R-induced injuries, endoplasmic reticulum stress (ERS)-related apoptosis is currently considered to be an important participant. Thus, in present study, we focused on the underlying mechanisms of I/R-induced AKI, and postulated that Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. METHODS: We established renal I/R models with Cx32(+/+) and Cx32(-/-) mice, which underwent double kidneys clamping and recanalization. ROS scavenger (N-acetylcysteine, NAC) and ERS inhibitors (4-phenyl butyric acid, 4-PBA, and tauroursodeoxycholic acid, TUDCA) were used to decrease the content of ROS and attenuate ERS activation, respectively. RESULTS: Renal damage was progressively exacerbated in a time-dependent manner at the reperfusion stage, that was consistent with the alternation of ERS activation, including glucose regulated protein 78 (BiP/GRP78), X box-binding protein1, and C/EBP homologous protein expression. TUDCA or 4-PBA application attenuated I/R-induced ERS activation and protected against renal tubular epithelial cells apoptosis and renal damage. Cx32 deficiency decreased ROS generation and distribution between the neighboring cells, which attenuated I/R-induced ERS activation, and improved cell apoptosis and renal damage. CONCLUSION: Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Cx32 deficiency, ROS elimination, and ERS inhibition all could protect against I/R-induced AKI. |*Apoptosis/drug effects [MESH] |*Endoplasmic Reticulum Stress/drug effects [MESH] |*Signal Transduction/drug effects [MESH] |Acetylcysteine/pharmacology [MESH] |Acute Kidney Injury/*etiology/*metabolism [MESH] |Animals [MESH] |Connexins/*metabolism [MESH] |Endoplasmic Reticulum Chaperone BiP [MESH] |Epithelial Cells/drug effects/pathology [MESH] |Gap Junction beta-1 Protein [MESH] |Gene Deletion [MESH] |Gene Knockout Techniques [MESH] |Kidney/pathology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Phenylbutyrates/pharmacology [MESH] |Reactive Oxygen Species/*metabolism [MESH] |Reperfusion Injury/*complications [MESH]Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum (epmc).pdf DeepDyve Pubget Overpricing