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10.1172/JCI121987 http://scihub22266oqcxt.onion/10.1172/JCI121987 30741721!6391108!30741721     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30741721&cmd=llinks): Failed to open stream: HTTP request failed! 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PTEN-induced partial epithelial-mesenchymal transition drives diabetic kidney disease |pdf=|usr=}}{{30741721}} gab.com Text PTEN-induced partial epithelial-mesenchymal transition drives diabetic kidney disease JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=30741721 #FOAvip Epithelial-mesenchymal transition (EMT) contributes significantly to interstitial matrix deposition in diabetic kidney disease (DKD). However, detection of EMT in kidney tissue is impracticable, and anti-EMT therapies have long been hindered. We reported that phosphatase and tensin homolog (PTEN) promoted transforming growth factor beta 1 (TGF-beta), sonic hedgehog (SHH), connective tissue growth factor (CTGF), interleukin 6 (IL-6), and hyperglycemia-induced EMT when PTEN was modified by a MEX3C-catalyzed K27-linked polyubiquitination at lysine 80 (referred to as PTENK27-polyUb). Genetic inhibition of PTENK27-polyUb alleviated Col4a3 knockout-, folic acid-, and streptozotocin-induced (STZ-induced) kidney injury. Serum and urine PTENK27-polyUb concentrations were negatively correlated with glomerular filtration rate (GFR) for diabetic patients. Mechanistically, PTENK27-polyUb facilitated dephosphorylation and protein stabilization of TWIST, SNAI1, and YAP in renal epithelial cells, leading to enhanced EMT. We identified that a small molecule, triptolide, inhibited MEX3C-catalyzed PTENK27-polyUb and EMT of renal epithelial cells. Treatment with triptolide reduced TWIST, SNAI1, and YAP concurrently and improved kidney health in Col4a3 knockout-, folic acid-injured disease models and STZ-induced, BTBR ob/ob diabetic nephropathy models. Hence, we demonstrated the important role of PTENK27-polyUb in DKD and a promising therapeutic strategy that inhibited the progression of DKD. Twit Text FOAVip PTEN-induced partial epithelial-mesenchymal transition drives diabetic kidney disease ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=30741721 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30741721 #FOAvip English Wikipedia <ref>{{Cite pmid|30741721}}</ref> PTEN-induced partial epithelial-mesenchymal transition drives diabetic kidney disease #MMPMID30741721 Li Y; Hu Q; Li C; Liang K; Xiang Y; Hsiao H; Nguyen TK; Park PK; Egranov SD; Ambati CR; Putluri N; Hawke DH; Han L; Hung MC; Danesh FR; Yang L; Lin C J Clin Invest 2019[Mar]; 129 (3): 1129-1151 PMID30741721show ga Epithelial-mesenchymal transition (EMT) contributes significantly to interstitial matrix deposition in diabetic kidney disease (DKD). However, detection of EMT in kidney tissue is impracticable, and anti-EMT therapies have long been hindered. We reported that phosphatase and tensin homolog (PTEN) promoted transforming growth factor beta 1 (TGF-beta), sonic hedgehog (SHH), connective tissue growth factor (CTGF), interleukin 6 (IL-6), and hyperglycemia-induced EMT when PTEN was modified by a MEX3C-catalyzed K27-linked polyubiquitination at lysine 80 (referred to as PTENK27-polyUb). Genetic inhibition of PTENK27-polyUb alleviated Col4a3 knockout-, folic acid-, and streptozotocin-induced (STZ-induced) kidney injury. Serum and urine PTENK27-polyUb concentrations were negatively correlated with glomerular filtration rate (GFR) for diabetic patients. Mechanistically, PTENK27-polyUb facilitated dephosphorylation and protein stabilization of TWIST, SNAI1, and YAP in renal epithelial cells, leading to enhanced EMT. We identified that a small molecule, triptolide, inhibited MEX3C-catalyzed PTENK27-polyUb and EMT of renal epithelial cells. Treatment with triptolide reduced TWIST, SNAI1, and YAP concurrently and improved kidney health in Col4a3 knockout-, folic acid-injured disease models and STZ-induced, BTBR ob/ob diabetic nephropathy models. Hence, we demonstrated the important role of PTENK27-polyUb in DKD and a promising therapeutic strategy that inhibited the progression of DKD. |*Epithelial-Mesenchymal Transition[MESH] |Adaptor Proteins, Signal Transducing/genetics/metabolism[MESH] |Animals[MESH] |Autoantigens/genetics/metabolism[MESH] |Cell Cycle Proteins/genetics/metabolism[MESH] |Cell Line[MESH] |Collagen Type IV/genetics/metabolism[MESH] |Diabetes Mellitus, Experimental/genetics/*metabolism/pathology[MESH] |Diabetic Nephropathies/genetics/*metabolism/pathology[MESH] |Humans[MESH] |Kidney/*metabolism/pathology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |PTEN Phosphohydrolase/genetics/*metabolism[MESH] |Snail Family Transcription Factors/genetics/metabolism[MESH] |Twist-Related Protein 1/genetics/metabolism[MESH]PTEN-induced partial epithelial-mesenchymal transition drives diabetic(epmc).pdf DeepDyve Pubget Overpricing