Angiotensin II induces expression of inflammatory mediators in vascular adventitial fibroblasts.
- Author:
Wen-Dong CHEN
1
;
Yu-Feng CHU
2
;
Xiao-Dong LI
1
;
Ping-Jin GAO
1
Author Information
1. State Key Laboratory of Medical Genomics and Shanghai Key Laboratory of Vascular Biology at Ruijin Hospital and Shanghai Institute of Hypertension, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
2. Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
- Publication Type:Journal Article
- MeSH:
Adventitia;
drug effects;
Angiotensin II;
pharmacology;
Animals;
Cell Line;
Chemokine CCL2;
metabolism;
Culture Media, Conditioned;
Fibroblasts;
drug effects;
immunology;
Inflammation;
immunology;
Intercellular Adhesion Molecule-1;
metabolism;
Interleukin-6;
metabolism;
Macrophages;
drug effects;
immunology;
Mice;
P-Selectin;
metabolism;
RAW 264.7 Cells;
Rats;
Up-Regulation
- From:
Acta Physiologica Sinica
2015;67(6):603-610
- CountryChina
- Language:Chinese
-
Abstract:
Vascular adventitial fibroblasts (AF) may play an important role in vascular inflammation. This study was aimed to investigate the expression pattern of inflammatory mediators in AF induced by angiotensin II (AngII) and to explore the effects of AF-derived inflammatory mediators on the adhesion and migration of macrophages both in vitro and in vivo. We used real-time RT-PCR to detect the mRNA expression of inflammatory mediators in cultured AF. The results showed that AngII (1 × 10(-7) mol/L) up-regulated mRNA expression of 4 inflammatory mediators, including P-selectin, ICAM-1, IL-6 and MCP-1, in cultured AF. Western blot analysis or ELISA revealed that AngII up-regulated P-selectin and ICAM-1 protein expression and IL-6 secretion in cultured AF, but did not alter MCP-1 secretion. We further detected the effects of AF-derived inflammatory mediators on the adhesion and chemotaxis of RAW264.7, a macrophage cell line. We found that AF stimulated with AngII could enhance the adhesion of RAW264.7 and the conditioned medium from AngII-stimulated AF could enhance the migration of RAW264.7. Immunofluorescence study showed an enhanced accumulation of CD68 positive cells and the up-regulation of P-selectin, ICAM-1, IL-6 and MCP-1 in aortic adventitia of AngII-infused (200 ng/kg per min for 2 weeks) rats. We concluded that AF may contribute to vascular inflammation via expression of certain inflammatory mediators and the subsequent adhesion and chemotaxis of macrophages.
