Serum Amyloid a Promotes Visfatin Expression in Macrophages
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...
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Online Access: | http://dx.doi.org/10.1155/2016/4819327 |
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doaj-5d330db600d04803803ce150194f1c2d2020-11-24T21:32:25ZengHindawi LimitedBioMed Research International2314-61332314-61412016-01-01201610.1155/2016/48193274819327Serum Amyloid a Promotes Visfatin Expression in MacrophagesShixun Wang0Xincai Zhang1Lei Tan2Department of Cardiology II, Weifang People’s Hospital, Weifang 261041, ChinaDepartment of Cardiology II, Weifang People’s Hospital, Weifang 261041, ChinaDepartment of Cardiology II, Weifang People’s Hospital, Weifang 261041, ChinaVisfatin 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-γ (PPAR-γ) 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-γ signaling pathway.http://dx.doi.org/10.1155/2016/4819327 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Shixun Wang Xincai Zhang Lei Tan |
spellingShingle |
Shixun Wang Xincai Zhang Lei Tan Serum Amyloid a Promotes Visfatin Expression in Macrophages BioMed Research International |
author_facet |
Shixun Wang Xincai Zhang Lei Tan |
author_sort |
Shixun Wang |
title |
Serum Amyloid a Promotes Visfatin Expression in Macrophages |
title_short |
Serum Amyloid a Promotes Visfatin Expression in Macrophages |
title_full |
Serum Amyloid a Promotes Visfatin Expression in Macrophages |
title_fullStr |
Serum Amyloid a Promotes Visfatin Expression in Macrophages |
title_full_unstemmed |
Serum Amyloid a Promotes Visfatin Expression in Macrophages |
title_sort |
serum amyloid a promotes visfatin expression in macrophages |
publisher |
Hindawi Limited |
series |
BioMed Research International |
issn |
2314-6133 2314-6141 |
publishDate |
2016-01-01 |
description |
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-γ (PPAR-γ) 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-γ signaling pathway. |
url |
http://dx.doi.org/10.1155/2016/4819327 |
work_keys_str_mv |
AT shixunwang serumamyloidapromotesvisfatinexpressioninmacrophages AT xincaizhang serumamyloidapromotesvisfatinexpressioninmacrophages AT leitan serumamyloidapromotesvisfatinexpressioninmacrophages |
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1725957636102291456 |