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10.1074/jbc.RA117.001032 http://scihub22266oqcxt.onion/10.1074/jbc.RA117.001032 C6139551!6139551 !30076216     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30076216 &cmd=llinks): Failed to open stream: HTTP request failed! 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TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis |pdf=|usr=}}{{30076216 }} gab.com Text TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=30076216 #FOAvip High-glucose (HG) levels and hyperglycemia associated with diabetes are known to cause neuronal damage. The detailed molecular mechanisms, however, remain to be elucidated. Here, we investigated the role of transient receptor potential melastatin 7 (TRPM7) channels in HG-mediated endoplasmic reticulum stress (ERS) and injury of NS20Y neuronal cells. The cells were incubated in the absence or presence of HG for 48 h. We found that mRNA and protein levels of TRPM7 and of ERS-associated proteins, such as C/EBP homologous protein (CHOP), 78-kDa glucose-regulated protein (GRP78), and inducible nitric-oxide synthase (iNOS), increased in HG-treated cells, along with significantly increased TRPM7-associated currents in these cells. Similar results were obtained in cerebral cortical tissue from an insulin-deficiency model of diabetic mice. Moreover, HG treatment of cells activated ERS-associated proapoptotic caspase activity and induced cellular injury. Interestingly, a NOS inhibitor, l-NAME, suppressed the HG-induced increase of TRPM7 expression and cellular injury. siRNA-mediated TRPM7 knockdown or chemical inhibition of TRPM7 activity also suppressed HG-induced ERS and decreased cleaved caspase-12/caspase-3 levels and cell injury. Of note, TRPM7 overexpression increased ERS and cell injury independently of its kinase activity. Taken together, our findings suggest that TRPM7 channel activities play a key role in HG-associated ERS and cytotoxicity through an apoptosis-inducing signaling cascade involving HG, iNOS, TRPM7, ERS proteins, and caspases. Twit Text FOAVip TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=30076216 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30076216 #FOAvip English Wikipedia <ref>{{Cite pmid|30076216 }}</ref> TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis #MMPMID30076216 Huang Y ; Leng TD ; Inoue K ; Yang T ; Liu M ; Horgen FD ; Fleig A ; Li J ; Xiong ZG J Biol Chem 2018[Sep]; 293 (37 ): 14393-14406 PMID30076216 show ga High-glucose (HG) levels and hyperglycemia associated with diabetes are known to cause neuronal damage. The detailed molecular mechanisms, however, remain to be elucidated. Here, we investigated the role of transient receptor potential melastatin 7 (TRPM7) channels in HG-mediated endoplasmic reticulum stress (ERS) and injury of NS20Y neuronal cells. The cells were incubated in the absence or presence of HG for 48 h. We found that mRNA and protein levels of TRPM7 and of ERS-associated proteins, such as C/EBP homologous protein (CHOP), 78-kDa glucose-regulated protein (GRP78), and inducible nitric-oxide synthase (iNOS), increased in HG-treated cells, along with significantly increased TRPM7-associated currents in these cells. Similar results were obtained in cerebral cortical tissue from an insulin-deficiency model of diabetic mice. Moreover, HG treatment of cells activated ERS-associated proapoptotic caspase activity and induced cellular injury. Interestingly, a NOS inhibitor, l-NAME, suppressed the HG-induced increase of TRPM7 expression and cellular injury. siRNA-mediated TRPM7 knockdown or chemical inhibition of TRPM7 activity also suppressed HG-induced ERS and decreased cleaved caspase-12/caspase-3 levels and cell injury. Of note, TRPM7 overexpression increased ERS and cell injury independently of its kinase activity. Taken together, our findings suggest that TRPM7 channel activities play a key role in HG-associated ERS and cytotoxicity through an apoptosis-inducing signaling cascade involving HG, iNOS, TRPM7, ERS proteins, and caspases. |Animals [MESH] |Apoptosis/*physiology [MESH] |Brain/metabolism [MESH] |Caspases/metabolism [MESH] |Diabetes Mellitus, Experimental/metabolism [MESH] |Endoplasmic Reticulum Chaperone BiP [MESH] |Endoplasmic Reticulum Stress/*physiology [MESH] |Glucose/*metabolism [MESH] |Heat-Shock Proteins/genetics/metabolism [MESH] |Insulin/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neurons/*cytology [MESH] |Nitric Oxide Synthase Type II/genetics/metabolism [MESH] |TRPM Cation Channels/genetics/metabolism/*physiology [MESH]TRPM7 channels play a role in high glucose-induced endoplasmic reticul(epmc).pdf DeepDyve Pubget Overpricing