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10.5534/wjmh.170005 http://scihub22266oqcxt.onion/10.5534/wjmh.170005 C5924955!5924955 !29706035     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29706035 &cmd=llinks): Failed to open stream: HTTP request failed! 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Silencing Histone Deacetylase 7 Alleviates Transforming Growth Factor-?1-Induced Profibrotic Responses in Fibroblasts Derived from Peyronie s Plaque |pdf=|usr=}}{{29706035 }} gab.com Text Silencing Histone Deacetylase 7 Alleviates Transforming Growth Factor- 1-Induced Profibrotic Responses in Fibroblasts Derived from Peyronie s Plaque JO: World J Mens Health http://www.kidney.de/pget.php?&tw=1&pmid=29706035 #FOAvip PURPOSE: Epigenetic modifications, such as histone acetylation/deacetylation and DNA methylation, play a crucial role in the pathogenesis of inflammatory disorders and fibrotic diseases. The aim of this study was to study the differential gene expression of histone deacetylases (HDACs) in fibroblasts isolated from plaque tissue of Peyronie's disease (PD) or normal tunica albuginea (TA) and to examine the anti-fibrotic effect of small interfering RNA (siRNA)-mediated silencing of HDAC7 in fibroblasts derived from human PD plaque. MATERIALS AND METHODS: For differential gene expression study, we performed reverse-transcriptase polymerase chain reaction for HDAC isoforms (1-11) in fibroblasts isolated from PD plaque or normal TA. Fibroblasts isolated from PD plaque were pretreated with HDAC7 siRNA (100 pmol) and then stimulated with transforming growth factor-?1 (TGF-?1, 10 ng/mL). Protein was extracted from treated fibroblasts for Western blotting. We also performed immunocytochemistry to detect the expression of extracellular matrix proteins and to examine the effect of HDAC2 siRNA on the TGF-?1-induced nuclear translocation of Smad2/3 and myofibroblastic differentiation. RESULTS: The mRNA expression of HDAC2, 3, 4, 5, 7, 8, 10, and 11 was higher in fibroblasts isolated from PD plaque than in fibroblasts isolated from normal TA tissue. Knockdown of HDAC7 in PD fibroblasts inhibited TGF-?1-induced nuclear shuttle of Smad2 and Smad3, transdifferentiation of fibroblasts into myofibroblasts, and abrogated TGF-?1-induced production of extracellular matrix protein. CONCLUSIONS: These findings suggest that specific inhibition of HDAC7 with RNA interference may represent a promising epigenetic therapy for PD. Twit Text FOAVip Silencing Histone Deacetylase 7 Alleviates Transforming Growth Factor- 1-Induced Profibrotic Responses in Fibroblasts Derived from Peyronie s Plaque ????World J Mens Health http://www.kidney.de/pget.php?&tw=1&pmid=29706035 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29706035 #FOAvip English Wikipedia <ref>{{Cite pmid|29706035 }}</ref> Silencing Histone Deacetylase 7 Alleviates Transforming Growth Factor-?1-Induced Profibrotic Responses in Fibroblasts Derived from Peyronie s Plaque #MMPMID29706035 Kang DH ; Yin GN ; Choi MJ ; Song KM ; Ghatak K ; Minh NN ; Kwon MH ; Seong DH ; Ryu JK ; Suh JK World J Mens Health 2018[May]; 36 (2 ): 139-146 PMID29706035 show ga PURPOSE: Epigenetic modifications, such as histone acetylation/deacetylation and DNA methylation, play a crucial role in the pathogenesis of inflammatory disorders and fibrotic diseases. The aim of this study was to study the differential gene expression of histone deacetylases (HDACs) in fibroblasts isolated from plaque tissue of Peyronie's disease (PD) or normal tunica albuginea (TA) and to examine the anti-fibrotic effect of small interfering RNA (siRNA)-mediated silencing of HDAC7 in fibroblasts derived from human PD plaque. MATERIALS AND METHODS: For differential gene expression study, we performed reverse-transcriptase polymerase chain reaction for HDAC isoforms (1-11) in fibroblasts isolated from PD plaque or normal TA. Fibroblasts isolated from PD plaque were pretreated with HDAC7 siRNA (100 pmol) and then stimulated with transforming growth factor-?1 (TGF-?1, 10 ng/mL). Protein was extracted from treated fibroblasts for Western blotting. We also performed immunocytochemistry to detect the expression of extracellular matrix proteins and to examine the effect of HDAC2 siRNA on the TGF-?1-induced nuclear translocation of Smad2/3 and myofibroblastic differentiation. RESULTS: The mRNA expression of HDAC2, 3, 4, 5, 7, 8, 10, and 11 was higher in fibroblasts isolated from PD plaque than in fibroblasts isolated from normal TA tissue. Knockdown of HDAC7 in PD fibroblasts inhibited TGF-?1-induced nuclear shuttle of Smad2 and Smad3, transdifferentiation of fibroblasts into myofibroblasts, and abrogated TGF-?1-induced production of extracellular matrix protein. CONCLUSIONS: These findings suggest that specific inhibition of HDAC7 with RNA interference may represent a promising epigenetic therapy for PD. äSilencing Histone Deacetylase 7 Alleviates Transforming Growth Factor-(epmc).pdf DeepDyve Pubget Overpricing