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10.3892/ijmm.2017.3327 http://scihub22266oqcxt.onion/10.3892/ijmm.2017.3327 C5819905!5819905 !29286065     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29286065 &cmd=llinks): Failed to open stream: HTTP request failed! 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Anti-inflammatory effects of Lefty-1 in renal tubulointerstitial inflammation via regulation of the NF-?B pathway |pdf=|usr=}}{{29286065 }} gab.com Text Anti-inflammatory effects of Lefty-1 in renal tubulointerstitial inflammation via regulation of the NF- B pathway JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29286065 #FOAvip Renal tubulointerstitial inflammation has an important role in fibrosis, which is the main pathogenetic alteration associated with chronic kidney disease (CKD). The left?right determination factor 1 (Lefty?1) gene pleiotropically and biologically regulates transforming growth factor, mitogen?activated protein kinase and other signaling pathways, and is considered to have a potential anti?inflammatory function. However, its role in renal tubulointerstitial inflammation, which is often a long?term consequence of renal fibrosis, is currently unknown. In the present study, the effects of adenovirus?mediated overexpression of Lefty?1 (Ad?Lefty?1?flag) on renal tubulointerstitial inflammation were determined using a mouse model of unilateral ureteral obstruction (UUO) and a rat renal tubular duct epithelial cell line (NRK?52E), which was treated with lipopolysaccharide (LPS). In vivo results indicated that the inflammatory response was increased in UUO mice, as evidenced by the increase in inflammatory cytokines and chemokines. Conversely, Lefty?1 significantly reversed the effects of UUO. Furthermore, the results of the in vitro study demonstrated that Lefty?1 significantly inhibited LPS?induced inflammatory marker expression in cultured NRK?52E cells via the nuclear factor (NF)??B signaling pathway. These results suggested that Lefty?1 may ameliorate renal tubulointerstitial inflammation by suppressing NF??B signaling. In conclusion, the findings of the present study indicated that Lefty?1 may be considered a potential novel therapeutic agent for inhibiting renal tubulointerstitial inflammation or even reversing the CKD process. Twit Text FOAVip Anti-inflammatory effects of Lefty-1 in renal tubulointerstitial inflammation via regulation of the NF- B pathway ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29286065 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29286065 #FOAvip English Wikipedia <ref>{{Cite pmid|29286065 }}</ref> Anti-inflammatory effects of Lefty-1 in renal tubulointerstitial inflammation via regulation of the NF-?B pathway #MMPMID29286065 Zhang L ; Xu C ; Hu W ; Wu P ; Qin C ; Zhang J Int J Mol Med 2018[Mar]; 41 (3 ): 1293-1304 PMID29286065 show ga Renal tubulointerstitial inflammation has an important role in fibrosis, which is the main pathogenetic alteration associated with chronic kidney disease (CKD). The left?right determination factor 1 (Lefty?1) gene pleiotropically and biologically regulates transforming growth factor, mitogen?activated protein kinase and other signaling pathways, and is considered to have a potential anti?inflammatory function. However, its role in renal tubulointerstitial inflammation, which is often a long?term consequence of renal fibrosis, is currently unknown. In the present study, the effects of adenovirus?mediated overexpression of Lefty?1 (Ad?Lefty?1?flag) on renal tubulointerstitial inflammation were determined using a mouse model of unilateral ureteral obstruction (UUO) and a rat renal tubular duct epithelial cell line (NRK?52E), which was treated with lipopolysaccharide (LPS). In vivo results indicated that the inflammatory response was increased in UUO mice, as evidenced by the increase in inflammatory cytokines and chemokines. Conversely, Lefty?1 significantly reversed the effects of UUO. Furthermore, the results of the in vitro study demonstrated that Lefty?1 significantly inhibited LPS?induced inflammatory marker expression in cultured NRK?52E cells via the nuclear factor (NF)??B signaling pathway. These results suggested that Lefty?1 may ameliorate renal tubulointerstitial inflammation by suppressing NF??B signaling. In conclusion, the findings of the present study indicated that Lefty?1 may be considered a potential novel therapeutic agent for inhibiting renal tubulointerstitial inflammation or even reversing the CKD process. |*Signal Transduction [MESH] |Actins/metabolism [MESH] |Adenoviridae/metabolism [MESH] |Animals [MESH] |Anti-Inflammatory Agents/*metabolism [MESH] |Cell Death [MESH] |Cell Nucleus/metabolism [MESH] |Collagen/metabolism [MESH] |Fibronectins/metabolism [MESH] |Inflammation Mediators/metabolism [MESH] |Inflammation/*metabolism/*pathology [MESH] |Kidney Tubules/*metabolism/*pathology [MESH] |Left-Right Determination Factors/genetics/*metabolism [MESH] |Lipopolysaccharides [MESH] |Macrophages/metabolism [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |NF-kappa B/*metabolism [MESH] |Protein Transport [MESH] |RNA, Messenger/genetics/metabolism [MESH] |Rats [MESH] |Smad7 Protein/metabolism [MESH]Anti-inflammatory effects of Lefty-1 in renal tubulointerstitial infla(epmc).pdf DeepDyve Pubget Overpricing