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10.1152/ajprenal.00234.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00234.2014 C4437003!4437003 !25428125     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25428125 &cmd=llinks): Failed to open stream: HTTP request failed! 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AMP-activated protein kinase (AMPK) activation inhibits nuclear translocation of Smad4 in mesangial cells and diabetic kidneys |pdf=|usr=}}{{25428125 }} gab.com Text AMP-activated protein kinase (AMPK) activation inhibits nuclear translocation of Smad4 in mesangial cells and diabetic kidneys JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25428125 #FOAvip Diabetic nephropathy is characterized by diffuse mesangial matrix expansion and is largely dependent on the TGF-?/Smad signaling pathway. Smad4 is required for TGF-? signaling; however, its regulation has not been well characterized in diabetic kidney disease. Here, we report that high glucose is sufficient to stimulate nuclear translocation of Smad4 in mesangial cells and that stimulation of the major energy sensor AMP-activated protein kinase (AMPK) has a potent effect to block Smad4 nuclear translocation. Activation of AMPK by 5-aminoimidazole-4-carboxamide-1-?-d-ribofuranoside (AICAR) inhibited high glucose-induced and TGF-? stimulation of nuclear Smad4. To identify which of the catalytic ?-subunits may be involved, small interfering (si) RNA-based inhibition of AMPK ?1- or ?2-subunit was employed. Inhibition of either subunit reduced overall AMPK activity and contributed to Smad4 nuclear accumulation. In an animal model of early diabetic kidney disease, induction of diabetes was found to markedly stimulate Smad4 protein levels and enhance nuclear accumulation. AMPK activation with AICAR completely prevented the upregulation of Smad4 and reduced mesangial matrix accumulation. We conclude that stimulation of Smad4 in cell culture and in in vivo models of early diabetic kidney disease is dependent on AMPK. Twit Text FOAVip AMP-activated protein kinase (AMPK) activation inhibits nuclear translocation of Smad4 in mesangial cells and diabetic kidneys ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25428125 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25428125 #FOAvip English Wikipedia <ref>{{Cite pmid|25428125 }}</ref> AMP-activated protein kinase (AMPK) activation inhibits nuclear translocation of Smad4 in mesangial cells and diabetic kidneys #MMPMID25428125 Zhao J ; Miyamoto S ; You YH ; Sharma K Am J Physiol Renal Physiol 2015[May]; 308 (10 ): F1167-77 PMID25428125 show ga Diabetic nephropathy is characterized by diffuse mesangial matrix expansion and is largely dependent on the TGF-?/Smad signaling pathway. Smad4 is required for TGF-? signaling; however, its regulation has not been well characterized in diabetic kidney disease. Here, we report that high glucose is sufficient to stimulate nuclear translocation of Smad4 in mesangial cells and that stimulation of the major energy sensor AMP-activated protein kinase (AMPK) has a potent effect to block Smad4 nuclear translocation. Activation of AMPK by 5-aminoimidazole-4-carboxamide-1-?-d-ribofuranoside (AICAR) inhibited high glucose-induced and TGF-? stimulation of nuclear Smad4. To identify which of the catalytic ?-subunits may be involved, small interfering (si) RNA-based inhibition of AMPK ?1- or ?2-subunit was employed. Inhibition of either subunit reduced overall AMPK activity and contributed to Smad4 nuclear accumulation. In an animal model of early diabetic kidney disease, induction of diabetes was found to markedly stimulate Smad4 protein levels and enhance nuclear accumulation. AMPK activation with AICAR completely prevented the upregulation of Smad4 and reduced mesangial matrix accumulation. We conclude that stimulation of Smad4 in cell culture and in in vivo models of early diabetic kidney disease is dependent on AMPK. |AMP-Activated Protein Kinases/drug effects/*metabolism [MESH] |Aminoimidazole Carboxamide/analogs & derivatives/pharmacology [MESH] |Animals [MESH] |Biological Transport/physiology [MESH] |Cell Line [MESH] |Cell Nucleus/*metabolism [MESH] |Diabetes Mellitus, Experimental/chemically induced/*complications [MESH] |Diabetic Nephropathies/*metabolism/pathology [MESH] |Disease Models, Animal [MESH] |Glucose/pharmacology [MESH] |Hypoglycemic Agents/pharmacology [MESH] |In Vitro Techniques [MESH] |Male [MESH] |Mesangial Cells/drug effects/*metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Ribonucleotides/pharmacology [MESH] |Signal Transduction/physiology [MESH] |Smad4 Protein/*antagonists & inhibitors/drug effects/*metabolism [MESH] |Streptozocin/adverse effects [MESH]AMP-activated protein kinase (AMPK) activation inhibits nuclear transl(epmc).pdf DeepDyve Pubget Overpricing