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10.1038/cddis.2017.552 http://scihub22266oqcxt.onion/10.1038/cddis.2017.552 C5680919!5680919 !29072686     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29072686 &cmd=llinks): Failed to open stream: HTTP request failed! 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Suppression of BMP-7 by histone deacetylase 2 promoted apoptosis of renal tubular epithelial cells in acute kidney injury |pdf=|usr=}}{{29072686 }} gab.com Text Suppression of BMP-7 by histone deacetylase 2 promoted apoptosis of renal tubular epithelial cells in acute kidney injury JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29072686 #FOAvip Cisplatin, a highly effective and widely used chemotherapeutic agent, has a major limitation for its nephrotoxicity. Currently, there are no therapies available to treat or prevent cisplatin nephrotoxicity. We recently identified a novel strategy for attenuating its nephrotoxicity in chemotherapy by histone deacetylase (HDAC) inhibitors via epigenetic modification to enhance bone morphogenetic protein 7 (BMP-7) expression. Cisplatin upregulated the activity of HDAC2 in the kidney. Inhibition of HDAC with clinically used trichostatin A (TSA) or valproic acid (VPA) suppressed cisplatin-induced kidney injury and epithelial cell apoptosis. Overexpression of HDAC2 promotes CP-treated tubular epithelium cells apoptosis. Chromatin immunoprecipitation assay clearly detected HDAC2 assosiation with BMP-7 promoter. Western blot and immunofluorescence results demonstrated that the expression of BMP-7 was clearly induced by TSA or VPA in vivo and in vitro. Interestingly, administration of recombinant BMP-7 (rhBMP-7) reduced cisplatin-induced kidney dysfunction. Moreover, BMP-7 treatment suppressed epithelial cell apoptosis and small interfering RNA-based knockdown of BMP-7 expression abolished HDAC inhibitors suppression of epithelial cell apoptosis in vitro. Results of current study indicated that TSA or VPA inhibited apoptosis of renal tubular epithelial cells via promoting the level of BMP-7 epigenetically through targeting HDAC2. Hence, HDAC inhibitors could be useful therapeutic agents for the prevention of cisplatin nephrotoxicity. Twit Text FOAVip Suppression of BMP-7 by histone deacetylase 2 promoted apoptosis of renal tubular epithelial cells in acute kidney injury ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29072686 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29072686 #FOAvip English Wikipedia <ref>{{Cite pmid|29072686 }}</ref> Suppression of BMP-7 by histone deacetylase 2 promoted apoptosis of renal tubular epithelial cells in acute kidney injury #MMPMID29072686 Ma T ; Huang C ; Xu Q ; Yang Y ; Liu Y ; Meng X ; Li J ; Ye M ; Liang H Cell Death Dis 2017[Oct]; 8 (10 ): e3139 PMID29072686 show ga Cisplatin, a highly effective and widely used chemotherapeutic agent, has a major limitation for its nephrotoxicity. Currently, there are no therapies available to treat or prevent cisplatin nephrotoxicity. We recently identified a novel strategy for attenuating its nephrotoxicity in chemotherapy by histone deacetylase (HDAC) inhibitors via epigenetic modification to enhance bone morphogenetic protein 7 (BMP-7) expression. Cisplatin upregulated the activity of HDAC2 in the kidney. Inhibition of HDAC with clinically used trichostatin A (TSA) or valproic acid (VPA) suppressed cisplatin-induced kidney injury and epithelial cell apoptosis. Overexpression of HDAC2 promotes CP-treated tubular epithelium cells apoptosis. Chromatin immunoprecipitation assay clearly detected HDAC2 assosiation with BMP-7 promoter. Western blot and immunofluorescence results demonstrated that the expression of BMP-7 was clearly induced by TSA or VPA in vivo and in vitro. Interestingly, administration of recombinant BMP-7 (rhBMP-7) reduced cisplatin-induced kidney dysfunction. Moreover, BMP-7 treatment suppressed epithelial cell apoptosis and small interfering RNA-based knockdown of BMP-7 expression abolished HDAC inhibitors suppression of epithelial cell apoptosis in vitro. Results of current study indicated that TSA or VPA inhibited apoptosis of renal tubular epithelial cells via promoting the level of BMP-7 epigenetically through targeting HDAC2. Hence, HDAC inhibitors could be useful therapeutic agents for the prevention of cisplatin nephrotoxicity. |Acute Kidney Injury/chemically induced/*metabolism/pathology/prevention & control [MESH] |Animals [MESH] |Bone Morphogenetic Protein 7/*antagonists & inhibitors/metabolism/pharmacology [MESH] |Cell Line [MESH] |Cisplatin/pharmacology [MESH] |Epithelial Cells/*metabolism [MESH] |Histone Deacetylase 2/antagonists & inhibitors/*metabolism [MESH] |Histone Deacetylase Inhibitors/pharmacology [MESH] |Humans [MESH] |Hydroxamic Acids/pharmacology [MESH] |Kidney Tubules/drug effects [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH]Suppression of BMP-7 by histone deacetylase 2 promoted apoptosis of re(epmc).pdf DeepDyve Pubget Overpricing