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10.12659/MSM.905642 http://scihub22266oqcxt.onion/10.12659/MSM.905642 C5881455!5881455!29572435     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       Med+Sci+Monit 2018 ; 24 (ä): 1724-32 Nephropedia Template TP {{tp|p=29572435|t=2018. ?-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/?-Catenin Pathway |pdf=|usr=}}{{29572435}} gab.com Text -Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/ -Catenin Pathway JO: Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29572435 #FOAvip Background: ?-arrestins have been shown to play a critical role in the progression of diabetic nephropathy. Nevertheless, the potential mechanism of ?-arrestins on the regulation of podocyte apoptosis has rarely been discussed. This study aimed to elucidate the regulation of ?-arrestin 1/2 on podocyte apoptosis through the Wnt/?-catenin pathway. Material/Methods: This study structured ?-arrestin 1/2 down-regulated and up-regulated expression by plasmid transfection. The protein levels were detected with Western blotting, and mRNA expression was detected with RT-qPCR. The apoptotic cells were measured by flow cytometry. Results: ?-arrestin 1/2 expression levels of podocytes were up-regulated in high-glucose-induced podocytes. ?-arrestin 1/2 overexpression inhibited the expression of nephrin and podocin protein. Up-regulated ?-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. Flow cytometry showed that the apoptotic cells were markedly higher in the ?-arrestin 1/2 up-regulated group compared with the scramble group. Expression of ?-catenin was increased in the ?-arrestin 1/2 up-regulated group, which indicated that the Wnt/?-catenin pathway was activated. Wnt/?-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by ?-arrestin 1/2 overexpression and high glucose. Conclusions: These results provide a molecular pathomechanism of ?-arrestin 1/2 and Wnt/?-catenin pathway on podocyte apoptosis and provide new ideas for the treatment of diabetic nephropathy, which paves the way for the future study of diabetic nephropathy and podocytes. Twit Text FOAVip -Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/ -Catenin Pathway ????Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29572435 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29572435 #FOAvip English Wikipedia <ref>{{Cite pmid|29572435}}</ref> ?-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/?-Catenin Pathway #MMPMID29572435 Wang Y; Li H; Song SP Med Sci Monit 2018[]; 24 (ä): 1724-32 PMID29572435show ga Background: ?-arrestins have been shown to play a critical role in the progression of diabetic nephropathy. Nevertheless, the potential mechanism of ?-arrestins on the regulation of podocyte apoptosis has rarely been discussed. This study aimed to elucidate the regulation of ?-arrestin 1/2 on podocyte apoptosis through the Wnt/?-catenin pathway. Material/Methods: This study structured ?-arrestin 1/2 down-regulated and up-regulated expression by plasmid transfection. The protein levels were detected with Western blotting, and mRNA expression was detected with RT-qPCR. The apoptotic cells were measured by flow cytometry. Results: ?-arrestin 1/2 expression levels of podocytes were up-regulated in high-glucose-induced podocytes. ?-arrestin 1/2 overexpression inhibited the expression of nephrin and podocin protein. Up-regulated ?-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. Flow cytometry showed that the apoptotic cells were markedly higher in the ?-arrestin 1/2 up-regulated group compared with the scramble group. Expression of ?-catenin was increased in the ?-arrestin 1/2 up-regulated group, which indicated that the Wnt/?-catenin pathway was activated. Wnt/?-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by ?-arrestin 1/2 overexpression and high glucose. Conclusions: These results provide a molecular pathomechanism of ?-arrestin 1/2 and Wnt/?-catenin pathway on podocyte apoptosis and provide new ideas for the treatment of diabetic nephropathy, which paves the way for the future study of diabetic nephropathy and podocytes. ä?-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy v(epmc).pdf DeepDyve Pubget Overpricing