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10.1016/j.kint.2016.09.042 http://scihub22266oqcxt.onion/10.1016/j.kint.2016.09.042 C5313320!5313320!27914709     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27914709&cmd=llinks): Failed to open stream: HTTP request failed! 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Podocyte-specific chemokine (C-C motif) receptor 2 overexpression mediates diabetic renal injury in mice |pdf=|usr=}}{{27914709}} gab.com Text Podocyte-specific chemokine (C-C motif) receptor 2 overexpression mediates diabetic renal injury in mice JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27914709 #FOAvip Inflammation is a central pathophysiologic mechanism that contributes to diabetes mellitus and diabetic nephropathy. Recently, we showed that macrophages directly contribute to diabetic renal injury, and that pharmacological blockade or genetic deficiency of chemokine (C-C motif) receptor 2 (CCR2) confers kidney protection in diabetic nephropathy. However, the direct role of CCR2 in kidney-derived cells such as podocytes in diabetic nephropathy remains unclear. To study this, we developed a transgenic mouse model expressing CCR2 specifically in podocytes (Tg(NPHS2-Ccr2)) on a nephropathy prone (DBA/2J) and CCR2 deficient (Ccr2?/?) background with heterozygous Ccr2+/? littermate controls. Diabetes was induced by streptozotocin. As expected, absence of CCR2 conferred kidney protection after nine weeks of diabetes. In contrast, transgenic CCR2 over expression in the podocytes of Ccr2?/? mice resulted in significantly increased albuminuria, blood urea nitrogen, histopathologic changes, kidney fibronectin and type-1 collagen expression, podocyte loss, and glomerular apoptosis after nine weeks of streptozotocin-induced diabetes. Interestingly, there was no concurrent increase in kidney macrophage recruitment or inflammatory cytokine levels in the mice. These findings support a direct role for CCR2 expression in podocytes to mediate diabetic renal injury, independent of monocyte/macrophage recruitment. Thus, targeting the CCR2 signaling cascade in podocytes could be a novel therapeutic approach for treatment of diabetic nephropathy. Twit Text FOAVip Podocyte-specific chemokine (C-C motif) receptor 2 overexpression mediates diabetic renal injury in mice ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27914709 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27914709 #FOAvip English Wikipedia <ref>{{Cite pmid|27914709}}</ref> Podocyte-specific chemokine (C-C motif) receptor 2 overexpression mediates diabetic renal injury in mice #MMPMID27914709 You H; Gao T; Raup-Konsavage WM; Cooper TK; Bronson SK; Reeves WB; Awad AS Kidney Int 2017[Mar]; 91 (3): 671-82 PMID27914709show ga Inflammation is a central pathophysiologic mechanism that contributes to diabetes mellitus and diabetic nephropathy. Recently, we showed that macrophages directly contribute to diabetic renal injury, and that pharmacological blockade or genetic deficiency of chemokine (C-C motif) receptor 2 (CCR2) confers kidney protection in diabetic nephropathy. However, the direct role of CCR2 in kidney-derived cells such as podocytes in diabetic nephropathy remains unclear. To study this, we developed a transgenic mouse model expressing CCR2 specifically in podocytes (Tg(NPHS2-Ccr2)) on a nephropathy prone (DBA/2J) and CCR2 deficient (Ccr2?/?) background with heterozygous Ccr2+/? littermate controls. Diabetes was induced by streptozotocin. As expected, absence of CCR2 conferred kidney protection after nine weeks of diabetes. In contrast, transgenic CCR2 over expression in the podocytes of Ccr2?/? mice resulted in significantly increased albuminuria, blood urea nitrogen, histopathologic changes, kidney fibronectin and type-1 collagen expression, podocyte loss, and glomerular apoptosis after nine weeks of streptozotocin-induced diabetes. Interestingly, there was no concurrent increase in kidney macrophage recruitment or inflammatory cytokine levels in the mice. These findings support a direct role for CCR2 expression in podocytes to mediate diabetic renal injury, independent of monocyte/macrophage recruitment. Thus, targeting the CCR2 signaling cascade in podocytes could be a novel therapeutic approach for treatment of diabetic nephropathy. äPodocyte-specific chemokine (C-C motif) receptor 2 overexpression medi(epmc).pdf DeepDyve Pubget Overpricing