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10.1016/j.bbagrm.2018.03.007 http://scihub22266oqcxt.onion/10.1016/j.bbagrm.2018.03.007 C5910054!5910054 !29555582     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29555582 &cmd=llinks): Failed to open stream: HTTP request failed! 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Suberanilohydroxamic acid prevents TGF-?1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation |pdf=|usr=}}{{29555582 }} gab.com Text Suberanilohydroxamic acid prevents TGF- 1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation JO: Biochim Biophys Acta Gene Regul Mech http://www.kidney.de/pget.php?&tw=1&pmid=29555582 #FOAvip Cyclooxygenase-2 (COX-2), with its main antifibrotic metabolite PGE(2), is regarded as an antifibrotic gene. Repressed COX-2 expression and deficient PGE(2) have been shown to contribute to the activation of lung fibroblasts and excessive deposition of collagen in pulmonary fibrosis. We have previously demonstrated that COX-2 expression in lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF) is epigenetically silenced and can be restored by epigenetic inhibitors. This study aimed to investigate whether COX-2 downregulation induced by the profibrotic cytokine transforming growth factor-?1 (TGF-?1) in normal lung fibroblasts could be prevented by epigenetic inhibitors. We found that COX-2 protein expression and PGE(2) production were markedly reduced by TGF-?1 and this was prevented by the pan-histone deacetylase inhibitor suberanilohydroxamic acid (SAHA) and to a lesser extent by the DNA demethylating agent Decitabine (DAC), but not by the G9a histone methyltransferase (HMT) inhibitor BIX01294 or the EZH2 HMT inhibitor 3-deazaneplanocin A (DZNep). However, chromatin immunoprecipitation assay revealed that the effect of SAHA was unlikely mediated by histone modifications. Instead 3'-untranslated region (3'-UTR) luciferase reporter assay indicated the involvement of post-transcriptional mechanisms. This was supported by the downregulation by SAHA of the 3'-UTR mRNA binding protein TIA-1 (T-cell intracellular antigen-1), a negative regulator of COX-2 translation. Furthermore, TIA-1 knockdown by siRNA mimicked the effect of SAHA on COX-2 expression. These findings suggest SAHA can prevent TGF-?1-induced COX-2 repression in lung fibroblasts post-transcriptionally through a novel TIA-1-dependent mechanism and provide new insights into the mechanisms underlying its potential antifibrotic activity. Twit Text FOAVip Suberanilohydroxamic acid prevents TGF- 1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation ????Biochim Biophys Acta Gene Regul Mech http://www.kidney.de/pget.php?&tw=1&pmid=29555582 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29555582 #FOAvip English Wikipedia <ref>{{Cite pmid|29555582 }}</ref> Suberanilohydroxamic acid prevents TGF-?1-induced COX-2 repression in human lung fibroblasts post-transcriptionally by TIA-1 downregulation #MMPMID29555582 Pasini A ; Brand OJ ; Jenkins G ; Knox AJ ; Pang L Biochim Biophys Acta Gene Regul Mech 2018[May]; 1861 (5 ): 463-472 PMID29555582 show ga Cyclooxygenase-2 (COX-2), with its main antifibrotic metabolite PGE(2), is regarded as an antifibrotic gene. Repressed COX-2 expression and deficient PGE(2) have been shown to contribute to the activation of lung fibroblasts and excessive deposition of collagen in pulmonary fibrosis. We have previously demonstrated that COX-2 expression in lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF) is epigenetically silenced and can be restored by epigenetic inhibitors. This study aimed to investigate whether COX-2 downregulation induced by the profibrotic cytokine transforming growth factor-?1 (TGF-?1) in normal lung fibroblasts could be prevented by epigenetic inhibitors. We found that COX-2 protein expression and PGE(2) production were markedly reduced by TGF-?1 and this was prevented by the pan-histone deacetylase inhibitor suberanilohydroxamic acid (SAHA) and to a lesser extent by the DNA demethylating agent Decitabine (DAC), but not by the G9a histone methyltransferase (HMT) inhibitor BIX01294 or the EZH2 HMT inhibitor 3-deazaneplanocin A (DZNep). However, chromatin immunoprecipitation assay revealed that the effect of SAHA was unlikely mediated by histone modifications. Instead 3'-untranslated region (3'-UTR) luciferase reporter assay indicated the involvement of post-transcriptional mechanisms. This was supported by the downregulation by SAHA of the 3'-UTR mRNA binding protein TIA-1 (T-cell intracellular antigen-1), a negative regulator of COX-2 translation. Furthermore, TIA-1 knockdown by siRNA mimicked the effect of SAHA on COX-2 expression. These findings suggest SAHA can prevent TGF-?1-induced COX-2 repression in lung fibroblasts post-transcriptionally through a novel TIA-1-dependent mechanism and provide new insights into the mechanisms underlying its potential antifibrotic activity. |Adenosine/administration & dosage/analogs & derivatives [MESH] |Azacitidine/administration & dosage/analogs & derivatives [MESH] |Cell Line [MESH] |Cyclooxygenase 1/genetics [MESH] |Cyclooxygenase 2/*genetics [MESH] |DNA Methylation/genetics [MESH] |Decitabine [MESH] |Enhancer of Zeste Homolog 2 Protein/genetics [MESH] |Fibroblasts/metabolism [MESH] |Gene Expression Regulation/genetics [MESH] |Histone Deacetylase Inhibitors/*administration & dosage [MESH] |Humans [MESH] |Hydroxamic Acids/administration & dosage [MESH] |Lung/drug effects/metabolism [MESH] |Promoter Regions, Genetic [MESH] |T-Cell Intracellular Antigen-1/*genetics [MESH] |Transforming Growth Factor beta1/*genetics [MESH]Suberanilohydroxamic acid prevents TGF-?1-induced COX-2 repression in (epmc).pdf DeepDyve Pubget Overpricing