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10.18632/oncotarget.13637 http://scihub22266oqcxt.onion/10.18632/oncotarget.13637 C5352066!5352066!27903964     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (1): 1429-37 Nephropedia Template TP {{tp|p=27903964|t=2017. LncRNA H19 inhibits autophagy by epigenetically silencing of DIRAS3 in diabetic cardiomyopathy |pdf=|usr=}}{{27903964}} gab.com Text LncRNA H19 inhibits autophagy by epigenetically silencing of DIRAS3 in diabetic cardiomyopathy JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27903964 #FOAvip We previously generated a rat model of diabetic cardiomyopathy and found that the expression of long non-coding RNA H19 was downregulated. The present study was aimed to explore the pathogenic role of H19 in the development of diabetic cardiomyopathy. Overexpression of H19 in diabetic rats attenuated cardiomyocyte autophagy and improved left ventricular function. High glucose was found to reduce H19 expression and increase autophagy in cultured neonatal cardiomyocytes. The results of RNA-binding protein immunoprecipitation showed that H19 could directly bind with EZH2 in cardiomyocytes. The chromatin immunoprecipitation assays indicated that H19 knockdown could reduce EZH2 occupancy and H3K27me3 binding in the promoter of DIRAS3. In addition, overexpression of H19 was found to downregulate DIRAS3 expression, promote mTOR phosphorylation and inhibit autophagy activation in cardiomyocytes exposed to high glucose. Furthermore, we also found that high glucose increased DIRAS3 expression in cardiomyocytes and DIRAS3 induced autophagy by inhibiting mTOR signaling. In conclusion, our study suggested that H19 could inhibit autophagy in cardiomyocytes by epigenetically silencing of DIRAS3, which might provide novel insights into understanding the molecular mechanisms of diabetic cardiomyopathy. Twit Text FOAVip LncRNA H19 inhibits autophagy by epigenetically silencing of DIRAS3 in diabetic cardiomyopathy ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27903964 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27903964 #FOAvip English Wikipedia <ref>{{Cite pmid|27903964}}</ref> LncRNA H19 inhibits autophagy by epigenetically silencing of DIRAS3 in diabetic cardiomyopathy #MMPMID27903964 Zhuo C; Jiang R; Lin X; Shao M Oncotarget 2017[Jan]; 8 (1): 1429-37 PMID27903964show ga We previously generated a rat model of diabetic cardiomyopathy and found that the expression of long non-coding RNA H19 was downregulated. The present study was aimed to explore the pathogenic role of H19 in the development of diabetic cardiomyopathy. Overexpression of H19 in diabetic rats attenuated cardiomyocyte autophagy and improved left ventricular function. High glucose was found to reduce H19 expression and increase autophagy in cultured neonatal cardiomyocytes. The results of RNA-binding protein immunoprecipitation showed that H19 could directly bind with EZH2 in cardiomyocytes. The chromatin immunoprecipitation assays indicated that H19 knockdown could reduce EZH2 occupancy and H3K27me3 binding in the promoter of DIRAS3. In addition, overexpression of H19 was found to downregulate DIRAS3 expression, promote mTOR phosphorylation and inhibit autophagy activation in cardiomyocytes exposed to high glucose. Furthermore, we also found that high glucose increased DIRAS3 expression in cardiomyocytes and DIRAS3 induced autophagy by inhibiting mTOR signaling. In conclusion, our study suggested that H19 could inhibit autophagy in cardiomyocytes by epigenetically silencing of DIRAS3, which might provide novel insights into understanding the molecular mechanisms of diabetic cardiomyopathy. äLncRNA H19 inhibits autophagy by epigenetically silencing of DIRAS3 in(epmc).pdf DeepDyve Pubget Overpricing