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10.1111/jcmm.13189 http://scihub22266oqcxt.onion/10.1111/jcmm.13189 C5661111!5661111 !28444861     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28444861 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Cell+Mol+Med 2017 ; 21 (11 ): 2732-2747 Nephropedia Template TP {{tp|p=28444861 |t=2017. LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with ?-catenin |pdf=|usr=}}{{28444861 }} gab.com Text LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with -catenin JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28444861 #FOAvip Metastasis associated lung adenocarcinoma transcript 1(MALAT1) is a long non-coding RNA, broadly expressed in mammalian tissues including kidney and up-regulated in a variety of cancer cells. To date, its functions in podocytes are largely unknown. ?-catenin is a key mediator in the canonical and non-canonical Wnt signalling pathway; its aberrant expression promotes podocyte malfunction and albuminuria, and contributes to kidney fibrosis. In this study, we found that MALAT1 levels were increased in kidney cortices from C57BL/6 mice with streptozocin (STZ)-induced diabetic nephropathy, and dynamically regulated in cultured mouse podocytes stimulated with high glucose, which showed a trend from rise to decline. The decline of MALAT1 levels was accompanied with ?-catenin translocation to the nuclei and enhanced expression of serine/arginine splicing factor 1 (SRSF1), a MALAT1 RNA-binding protein. Further we showed early interference with MALAT1 siRNA partially restored podocytes function and prohibited ?-catenin nuclear accumulation and SRSF1 overexpression. Intriguingly, we showed that ?-catenin was involved in MALAT1 transcription by binding to the promotor region of MALAT1; ?-catenin knock-down also decreased MALAT1 levels, suggesting a novel feedback regulation between MALAT1 and ?-catenin. Notably, ?-catenin deletion had limited effects on SRSF1 expression, demonstrating ?-catenin might serve as a downstream signal of SRSF1. These findings provided evidence for a pivotal role of MALAT1 in diabetic nephropathy and high glucose-induced podocyte damage. Twit Text FOAVip LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with -catenin ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28444861 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28444861 #FOAvip English Wikipedia <ref>{{Cite pmid|28444861 }}</ref> LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose-induced podocyte injury via its interplay with ?-catenin #MMPMID28444861 Hu M ; Wang R ; Li X ; Fan M ; Lin J ; Zhen J ; Chen L ; Lv Z J Cell Mol Med 2017[Nov]; 21 (11 ): 2732-2747 PMID28444861 show ga Metastasis associated lung adenocarcinoma transcript 1(MALAT1) is a long non-coding RNA, broadly expressed in mammalian tissues including kidney and up-regulated in a variety of cancer cells. To date, its functions in podocytes are largely unknown. ?-catenin is a key mediator in the canonical and non-canonical Wnt signalling pathway; its aberrant expression promotes podocyte malfunction and albuminuria, and contributes to kidney fibrosis. In this study, we found that MALAT1 levels were increased in kidney cortices from C57BL/6 mice with streptozocin (STZ)-induced diabetic nephropathy, and dynamically regulated in cultured mouse podocytes stimulated with high glucose, which showed a trend from rise to decline. The decline of MALAT1 levels was accompanied with ?-catenin translocation to the nuclei and enhanced expression of serine/arginine splicing factor 1 (SRSF1), a MALAT1 RNA-binding protein. Further we showed early interference with MALAT1 siRNA partially restored podocytes function and prohibited ?-catenin nuclear accumulation and SRSF1 overexpression. Intriguingly, we showed that ?-catenin was involved in MALAT1 transcription by binding to the promotor region of MALAT1; ?-catenin knock-down also decreased MALAT1 levels, suggesting a novel feedback regulation between MALAT1 and ?-catenin. Notably, ?-catenin deletion had limited effects on SRSF1 expression, demonstrating ?-catenin might serve as a downstream signal of SRSF1. These findings provided evidence for a pivotal role of MALAT1 in diabetic nephropathy and high glucose-induced podocyte damage. |Animals [MESH] |Cell Line, Transformed [MESH] |Diabetes Mellitus, Experimental/chemically induced/*genetics/metabolism/pathology [MESH] |Diabetic Nephropathies/chemically induced/*genetics/metabolism/pathology [MESH] |Feedback, Physiological [MESH] |Gene Expression Regulation [MESH] |Glucose/toxicity [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Podocytes/drug effects/metabolism/pathology [MESH] |Promoter Regions, Genetic [MESH] |Protein Binding [MESH] |Protein Transport [MESH] |RNA, Long Noncoding/antagonists & inhibitors/*genetics/metabolism [MESH] |RNA, Small Interfering/genetics/metabolism [MESH] |Serine-Arginine Splicing Factors/antagonists & inhibitors/*genetics/metabolism [MESH] |Streptozocin/toxicity [MESH] |Wnt Signaling Pathway [MESH]LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in (epmc).pdf DeepDyve Pubget Overpricing