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10.1371/journal.pone.0178147 http://scihub22266oqcxt.onion/10.1371/journal.pone.0178147 C5443579!5443579 !28542370     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28542370 &cmd=llinks): Failed to open stream: HTTP request failed! 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Upregulation of TLR4 via PKC activation contributes to impaired wound healing in high-glucose-treated kidney proximal tubular cells |pdf=|usr=}}{{28542370 }} gab.com Text Upregulation of TLR4 via PKC activation contributes to impaired wound healing in high-glucose-treated kidney proximal tubular cells JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28542370 #FOAvip Acute kidney injury (AKI) leads to a worse prognosis in diabetic patients compared with prognoses in non-diabetic patients, but whether and how diabetes affects kidney repair after AKI remains unknown. Here, we used scratch-wound healing and transwell migration models to examine whether and how wound healing is affected by high glucose levels in cultured kidney proximal tubular cells (RPTC). The results show that scratch-wound healing and transwell migration were significantly slower in high-glucose-treated kidney tubular cells (30 mM glucose) than in low-glucose-treated cells (5.5 mM). Toll-like receptor 4 (TLR4), MyD88, phospho-protein kinase C (PKC), phospho-p38 MAPK and monocyte chemoattractant protein-1 (MCP-1) mRNA levels were upregulated after high glucose treatments. Staurosporine, a selective PKC inhibitor, inhibited TLR4, MyD88 and p-p38 upregulation in the high-glucose-treated cells, indicating the involvement of PKC in high-glucose-induced TLR4 upregulation. The pharmacological inhibition of TLR4 or shRNA-mediated TLR4 knockdown improved wound healing and transwell migration in high-glucose-treated RPTC. In contrast, the overexpression of TLR4 in low-glucose-treated RPTC suppressed wound healing, mimicking the effects of high glucose levels. These results suggest that the upregulation of TLR4 expression via PKC activation contributes to defective wound healing in high-glucose-treated kidney tubular cells. Twit Text FOAVip Upregulation of TLR4 via PKC activation contributes to impaired wound healing in high-glucose-treated kidney proximal tubular cells ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28542370 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28542370 #FOAvip English Wikipedia <ref>{{Cite pmid|28542370 }}</ref> Upregulation of TLR4 via PKC activation contributes to impaired wound healing in high-glucose-treated kidney proximal tubular cells #MMPMID28542370 Peng J ; Zheng H ; Wang X ; Cheng Z PLoS One 2017[]; 12 (5 ): e0178147 PMID28542370 show ga Acute kidney injury (AKI) leads to a worse prognosis in diabetic patients compared with prognoses in non-diabetic patients, but whether and how diabetes affects kidney repair after AKI remains unknown. Here, we used scratch-wound healing and transwell migration models to examine whether and how wound healing is affected by high glucose levels in cultured kidney proximal tubular cells (RPTC). The results show that scratch-wound healing and transwell migration were significantly slower in high-glucose-treated kidney tubular cells (30 mM glucose) than in low-glucose-treated cells (5.5 mM). Toll-like receptor 4 (TLR4), MyD88, phospho-protein kinase C (PKC), phospho-p38 MAPK and monocyte chemoattractant protein-1 (MCP-1) mRNA levels were upregulated after high glucose treatments. Staurosporine, a selective PKC inhibitor, inhibited TLR4, MyD88 and p-p38 upregulation in the high-glucose-treated cells, indicating the involvement of PKC in high-glucose-induced TLR4 upregulation. The pharmacological inhibition of TLR4 or shRNA-mediated TLR4 knockdown improved wound healing and transwell migration in high-glucose-treated RPTC. In contrast, the overexpression of TLR4 in low-glucose-treated RPTC suppressed wound healing, mimicking the effects of high glucose levels. These results suggest that the upregulation of TLR4 expression via PKC activation contributes to defective wound healing in high-glucose-treated kidney tubular cells. |Animals [MESH] |Cell Movement/drug effects/physiology [MESH] |Cells, Cultured [MESH] |Gene Knockdown Techniques [MESH] |Glucose/*metabolism/pharmacology [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Kidney Tubules, Proximal/cytology/drug effects/*metabolism [MESH] |Protein Kinase C/*metabolism [MESH] |RNA, Messenger/genetics/metabolism [MESH] |Rats [MESH] |Toll-Like Receptor 4/antagonists & inhibitors/genetics/*metabolism [MESH] |Up-Regulation [MESH]Upregulation of TLR4 via PKC activation contributes to impaired wound (epmc).pdf DeepDyve Pubget Overpricing