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10.1159/000442051 http://scihub22266oqcxt.onion/10.1159/000442051 C4687741!4687741 !26613578     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26613578 &cmd=llinks): Failed to open stream: HTTP request failed! 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TGF?-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism |pdf=|usr=}}{{26613578 }} gab.com Text TGF -Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism JO: Nephron http://www.kidney.de/pget.php?&tw=1&pmid=26613578 #FOAvip BACKGROUND/AIMS: In podocytes, the overexpression of TGF? ligands and receptors during glomerulosclerosis could be a causal factor for injury induction and perpetuation in glomerular tufts. Mitochondrial dysfunction and oxidative stress are emerging as potential therapeutic targets in glomerular injury, and TGF? has been shown to modulate mitochondrial metabolism in different cell types. This study aims at investigating the role of TGF? in podocyte energy metabolism and cytoskeleton dynamics. METHODS: Mitochondrial function and cytoskeleton dynamics were analyzed in TGF?-treated WT and Smad2/3 double KO podocytes. RESULTS: TGF? treatment in podocytes induced a significant Smad-dependent increase of mitochondrial oxygen consumption rate (OCR). ATP content was unchanged and increased respiration was not associated with increased mitochondrial mass. Increased cellular reactive oxygen species induced by Smad-mediated TGF? signaling were reverted by NADPH oxidase inhibitor apocynin. TGF? treatment did not induce mitochondrial oxidative stress, and Smad2/3-dependent TGF? signaling and increased mitochondrial OCR were found to be associated with actin cytoskeleton dynamics. The role of motor proteins myosin II and dynamin in TGF?-induced actin polymerization was demonstrated by specific inhibition, resulting in actin stabilization and normalization of mitochondrial OCR. CONCLUSION: TGF?-induced rearrangements of actin cytoskeleton are controlled by Smad2/3 signaling pathways and coupled with the activation of mitochondrial ATP synthesis as bioenergetic adaptation to ATP consumption by ATP- and GTP-dependent motor proteins, myosin II and dynamin. Twit Text FOAVip TGF -Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism ????Nephron http://www.kidney.de/pget.php?&tw=1&pmid=26613578 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26613578 #FOAvip English Wikipedia <ref>{{Cite pmid|26613578 }}</ref> TGF?-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism #MMPMID26613578 Casalena G ; Bottinger E ; Daehn I Nephron 2015[]; 131 (4 ): 278-84 PMID26613578 show ga BACKGROUND/AIMS: In podocytes, the overexpression of TGF? ligands and receptors during glomerulosclerosis could be a causal factor for injury induction and perpetuation in glomerular tufts. Mitochondrial dysfunction and oxidative stress are emerging as potential therapeutic targets in glomerular injury, and TGF? has been shown to modulate mitochondrial metabolism in different cell types. This study aims at investigating the role of TGF? in podocyte energy metabolism and cytoskeleton dynamics. METHODS: Mitochondrial function and cytoskeleton dynamics were analyzed in TGF?-treated WT and Smad2/3 double KO podocytes. RESULTS: TGF? treatment in podocytes induced a significant Smad-dependent increase of mitochondrial oxygen consumption rate (OCR). ATP content was unchanged and increased respiration was not associated with increased mitochondrial mass. Increased cellular reactive oxygen species induced by Smad-mediated TGF? signaling were reverted by NADPH oxidase inhibitor apocynin. TGF? treatment did not induce mitochondrial oxidative stress, and Smad2/3-dependent TGF? signaling and increased mitochondrial OCR were found to be associated with actin cytoskeleton dynamics. The role of motor proteins myosin II and dynamin in TGF?-induced actin polymerization was demonstrated by specific inhibition, resulting in actin stabilization and normalization of mitochondrial OCR. CONCLUSION: TGF?-induced rearrangements of actin cytoskeleton are controlled by Smad2/3 signaling pathways and coupled with the activation of mitochondrial ATP synthesis as bioenergetic adaptation to ATP consumption by ATP- and GTP-dependent motor proteins, myosin II and dynamin. |*Adaptation, Physiological [MESH] |*Energy Metabolism [MESH] |Actin Cytoskeleton/*drug effects/metabolism [MESH] |Adenosine Triphosphate/biosynthesis [MESH] |Animals [MESH] |Cells, Cultured [MESH] |Mice [MESH] |Mitochondria/*metabolism [MESH] |Podocytes/*drug effects/metabolism [MESH] |Reactive Oxygen Species/metabolism [MESH] |Signal Transduction [MESH] |Smad Proteins/physiology [MESH]TGF?-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associat(epmc).pdf DeepDyve Pubget Overpricing