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10.1038/cddis.2014.466 http://scihub22266oqcxt.onion/10.1038/cddis.2014.466 C4649539!4649539!25356875     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       Cell+Death+Dis 2014 ; 5 (10): e1506- Nephropedia Template TP {{tp|p=25356875|t=2014. Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus |pdf=|usr=}}{{25356875}} gab.com Text Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25356875 #FOAvip Long noncoding RNAs (lncRNAs) have important roles in diverse biological processes. Our previous study has revealed that lncRNA-MALAT1 deregulation is implicated in the pathogenesis of diabetes-related microvascular disease, diabetic retinopathy (DR). However, the role of MALAT1 in retinal vasculature remodeling still remains elusive. Here we show that MALAT1 expression is significantly upregulated in the retinas of STZ-induced diabetic rats and db/db mice. MALAT1 knockdown could obviously ameliorate DR in vivo, as shown by pericyte loss, capillary degeneration, microvascular leakage, and retinal inflammation. Moreover, MALAT1 knockdown could regulate retinal endothelial cell proliferation, migration, and tube formation in vitro. The crosstalk between MALAT1 and p38 MAPK signaling pathway is involved in the regulation of endothelial cell function. MALAT1 upregulation represents a critical pathogenic mechanism for diabetes-induced microvascular dysfunction. Inhibition of MALAT1 may serve as a potential target for anti-angiogenic therapy for diabetes-related microvascular complications. Twit Text FOAVip Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=25356875 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25356875 #FOAvip English Wikipedia <ref>{{Cite pmid|25356875}}</ref> Pathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in diabetes mellitus #MMPMID25356875 Liu JY; Yao J; Li XM; Song YC; Wang XQ; Li YJ; Yan B; Jiang Q Cell Death Dis 2014[Oct]; 5 (10): e1506- PMID25356875show ga Long noncoding RNAs (lncRNAs) have important roles in diverse biological processes. Our previous study has revealed that lncRNA-MALAT1 deregulation is implicated in the pathogenesis of diabetes-related microvascular disease, diabetic retinopathy (DR). However, the role of MALAT1 in retinal vasculature remodeling still remains elusive. Here we show that MALAT1 expression is significantly upregulated in the retinas of STZ-induced diabetic rats and db/db mice. MALAT1 knockdown could obviously ameliorate DR in vivo, as shown by pericyte loss, capillary degeneration, microvascular leakage, and retinal inflammation. Moreover, MALAT1 knockdown could regulate retinal endothelial cell proliferation, migration, and tube formation in vitro. The crosstalk between MALAT1 and p38 MAPK signaling pathway is involved in the regulation of endothelial cell function. MALAT1 upregulation represents a critical pathogenic mechanism for diabetes-induced microvascular dysfunction. Inhibition of MALAT1 may serve as a potential target for anti-angiogenic therapy for diabetes-related microvascular complications. äPathogenic role of lncRNA-MALAT1 in endothelial cell dysfunction in di(epmc).pdf DeepDyve Pubget Overpricing