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10.1038/cddis.2015.220 http://scihub22266oqcxt.onion/10.1038/cddis.2015.220 C4558511!4558511 !26247729     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26247729 &cmd=llinks): Failed to open stream: HTTP request failed! 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Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study |pdf=|usr=}}{{26247729 }} gab.com Text Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=26247729 #FOAvip In the central nervous system (CNS), hyperglycemia leads to neuronal damage and cognitive decline. Recent research has focused on revealing alterations in the brain in hyperglycemia and finding therapeutic solutions for alleviating the hyperglycemia-induced cognitive dysfunction. Adiponectin is a protein hormone with a major regulatory role in diabetes and obesity; however, its role in the CNS has not been studied yet. Although the presence of adiponectin receptors has been reported in the CNS, adiponectin receptor-mediated signaling in the CNS has not been investigated. In the present study, we investigated adiponectin receptor (AdipoR)-mediated signaling in vivo using a high-fat diet and in vitro using neural stem cells (NSCs). We showed that AdipoR1 protects cell damage and synaptic dysfunction in the mouse brain in hyperglycemia. At high glucose concentrations in vitro, AdipoR1 regulated the survival of NSCs through the p53/p21 pathway and the proliferation- and differentiation-related factors of NSCs via tailless (TLX). Hence, we suggest that further investigations are necessary to understand the cerebral AdipoR1-mediated signaling in hyperglycemic conditions, because the modulation of AdipoR1 might alleviate hyperglycemia-induced neuropathogenesis. Twit Text FOAVip Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=26247729 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26247729 #FOAvip English Wikipedia <ref>{{Cite pmid|26247729 }}</ref> Adiponectin receptor-mediated signaling ameliorates cerebral cell damage and regulates the neurogenesis of neural stem cells at high glucose concentrations: an in vivo and in vitro study #MMPMID26247729 Song J ; Kang SM ; Kim E ; Kim CH ; Song HT ; Lee JE Cell Death Dis 2015[Aug]; 6 (8 ): e1844 PMID26247729 show ga In the central nervous system (CNS), hyperglycemia leads to neuronal damage and cognitive decline. Recent research has focused on revealing alterations in the brain in hyperglycemia and finding therapeutic solutions for alleviating the hyperglycemia-induced cognitive dysfunction. Adiponectin is a protein hormone with a major regulatory role in diabetes and obesity; however, its role in the CNS has not been studied yet. Although the presence of adiponectin receptors has been reported in the CNS, adiponectin receptor-mediated signaling in the CNS has not been investigated. In the present study, we investigated adiponectin receptor (AdipoR)-mediated signaling in vivo using a high-fat diet and in vitro using neural stem cells (NSCs). We showed that AdipoR1 protects cell damage and synaptic dysfunction in the mouse brain in hyperglycemia. At high glucose concentrations in vitro, AdipoR1 regulated the survival of NSCs through the p53/p21 pathway and the proliferation- and differentiation-related factors of NSCs via tailless (TLX). Hence, we suggest that further investigations are necessary to understand the cerebral AdipoR1-mediated signaling in hyperglycemic conditions, because the modulation of AdipoR1 might alleviate hyperglycemia-induced neuropathogenesis. |Animals [MESH] |Cell Differentiation [MESH] |Cell Proliferation [MESH] |Cell Survival [MESH] |Cerebral Cortex/drug effects/metabolism/pathology [MESH] |Cyclin-Dependent Kinase Inhibitor p21/*genetics/metabolism [MESH] |Diet, High-Fat/adverse effects [MESH] |Gene Expression Regulation [MESH] |Glucose/*toxicity [MESH] |Humans [MESH] |Hyperglycemia/etiology/*genetics/metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neural Stem Cells [MESH] |Neurogenesis/drug effects/genetics [MESH] |Primary Cell Culture [MESH] |Receptors, Adiponectin/*genetics/metabolism [MESH] |Receptors, Cytoplasmic and Nuclear/*genetics/metabolism [MESH] |Signal Transduction [MESH] |Synapses/drug effects/metabolism/pathology [MESH]Adiponectin receptor-mediated signaling ameliorates cerebral cell dama(epmc).pdf DeepDyve Pubget Overpricing