Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.bbagrm.2018.03.007 http://scihub22266oqcxt.onion/10.1016/j.bbagrm.2018.03.007 C5910054!5910054!29555582     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2018 ; 1861 (5): 463-72 Nephropedia Template TP {{tp|p=29555582|t=2018. 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 http://www.kidney.de/pget.php?&tw=1&pmid=29555582 #FOAvip Cyclooxygenase-2 (COX-2), with its main antifibrotic metabolite PGE2, is regarded as an antifibrotic gene. Repressed COX-2 expression and deficient PGE2 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 PGE2 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. Abbreviations: Unlabelled TableSAHAsuberanilohydroxamic acidTGF-?1transforming growth factor-?1COX-2cyclooxygenase-2TIA-1T-cell intracellular antigen-1PGE2prostaglandin E2IPFidiopathic pulmonary fibrosisDACDecitabineHMThistone methyltransferaseEZH2enhancer of zeste homolog 2DZNep3-deazaneplanocin A3?-UTR3?-untranslated region?-SMA?-smooth muscle actinECMextracellular matrixCOL1collagen 1DNMTDNA methyltransferaseHAThistone acetyltransferaseHDAChistone deacetylaseH3K9me3histone H3 lysine 9 trimethylationAREAUUUA-rich elementHuRhuman antigen RELAV1ELAV-like RNA binding protein 1TTPTristetraprolinCUGBP2CUG triplet repeat, RNA binding protein 2F-NLfibroblast from non-fibrotic lungFCSfetal calf serum 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 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 2018[May]; 1861 (5): 463-72 PMID29555582show ga Cyclooxygenase-2 (COX-2), with its main antifibrotic metabolite PGE2, is regarded as an antifibrotic gene. Repressed COX-2 expression and deficient PGE2 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 PGE2 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. Abbreviations: Unlabelled TableSAHAsuberanilohydroxamic acidTGF-?1transforming growth factor-?1COX-2cyclooxygenase-2TIA-1T-cell intracellular antigen-1PGE2prostaglandin E2IPFidiopathic pulmonary fibrosisDACDecitabineHMThistone methyltransferaseEZH2enhancer of zeste homolog 2DZNep3-deazaneplanocin A3?-UTR3?-untranslated region?-SMA?-smooth muscle actinECMextracellular matrixCOL1collagen 1DNMTDNA methyltransferaseHAThistone acetyltransferaseHDAChistone deacetylaseH3K9me3histone H3 lysine 9 trimethylationAREAUUUA-rich elementHuRhuman antigen RELAV1ELAV-like RNA binding protein 1TTPTristetraprolinCUGBP2CUG triplet repeat, RNA binding protein 2F-NLfibroblast from non-fibrotic lungFCSfetal calf serum äSuberanilohydroxamic acid prevents TGF-?1-induced COX-2 repression in (epmc).pdf DeepDyve Pubget Overpricing