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10.1155/2016/4819327 http://scihub22266oqcxt.onion/10.1155/2016/4819327 C4783535!4783535!27006946     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biomed+Res+Int 2016 ; 2016 (ä): ä Nephropedia Template TP {{tp|p=27006946|t=2016. Serum Amyloid a Promotes Visfatin Expression in Macrophages |pdf=|usr=}}{{27006946}} gab.com Text Serum Amyloid a Promotes Visfatin Expression in Macrophages JO: Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=27006946 #FOAvip Visfatin has been reported to exert an important role in the development of atherosclerosis. However, the mechanism that regulated the expression of Visfatin has not been elucidated yet. This study aimed to investigate the effect of SAA on the regulation of Visfatin, as well as the potential pathway. After RAW264.7 macrophages and primary monocytes were stimulated with SAA, the mRNA and protein expression of Visfatin was detected with real-time PCR and western blot, respectively. The concentration of Visfatin in the supernatant was measured with ELISA. Formyl peptide receptor 2 (FPR2) agonist (WKYMVm) and inhibitor (WRW4), extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor (PD98059), and peroxisome proliferator-activated receptor-? (PPAR-?) agonist (Rosiglitazone) and inhibitor (GW9662) were used to investigate the mechanism of regulation of Visfatin. The results demonstrated that SAA upregulated Visfatin expression in cultured RAW264.7 macrophages and in the primary monocytes. WRW4 decreased SAA-induced Visfatin production, while WKYMVm could induce Visfatin expression. PD98059 reduced SAA-induced Visfatin production. What is more, GW9662 inhibited SAA-induced Visfatin production, while Rosiglitazone promoted Visfatin expression. These results demonstrate that SAA upregulates Visfatin expression via a FPR2/ERK1/2/PPAR-? signaling pathway. Twit Text FOAVip Serum Amyloid a Promotes Visfatin Expression in Macrophages ????Biomed Res Int http://www.kidney.de/pget.php?&tw=1&pmid=27006946 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27006946 #FOAvip English Wikipedia <ref>{{Cite pmid|27006946}}</ref> Serum Amyloid a Promotes Visfatin Expression in Macrophages #MMPMID27006946 Wang S; Zhang X; Tan L Biomed Res Int 2016[]; 2016 (ä): ä PMID27006946show ga Visfatin has been reported to exert an important role in the development of atherosclerosis. However, the mechanism that regulated the expression of Visfatin has not been elucidated yet. This study aimed to investigate the effect of SAA on the regulation of Visfatin, as well as the potential pathway. After RAW264.7 macrophages and primary monocytes were stimulated with SAA, the mRNA and protein expression of Visfatin was detected with real-time PCR and western blot, respectively. The concentration of Visfatin in the supernatant was measured with ELISA. Formyl peptide receptor 2 (FPR2) agonist (WKYMVm) and inhibitor (WRW4), extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor (PD98059), and peroxisome proliferator-activated receptor-? (PPAR-?) agonist (Rosiglitazone) and inhibitor (GW9662) were used to investigate the mechanism of regulation of Visfatin. The results demonstrated that SAA upregulated Visfatin expression in cultured RAW264.7 macrophages and in the primary monocytes. WRW4 decreased SAA-induced Visfatin production, while WKYMVm could induce Visfatin expression. PD98059 reduced SAA-induced Visfatin production. What is more, GW9662 inhibited SAA-induced Visfatin production, while Rosiglitazone promoted Visfatin expression. These results demonstrate that SAA upregulates Visfatin expression via a FPR2/ERK1/2/PPAR-? signaling pathway. äSerum Amyloid a Promotes Visfatin Expression in Macrophages (epmc).pdf DeepDyve Pubget Overpricing