Angiotensin II induces the secretion of ICAM-1 and MCP-1 in human airway smooth muscle cells in vitro

Abstract

Background: Angiotensin [1] II is known to cause human airway smooth muscle (HASM) contraction and closely relate to asthma, however, the effect of Ang II on HASM cells (HASMCs) secretion function is still unclear. Methods: Primary cultured HASMCs were treated with Ang II, Ang II + Ang-(1–7), and Ang II + irbersatan (IRB), respectively. The nuclear translocation of the NF-κB p65 in HASMCs in each group was analyzed performed with Immunofluorescence. The expression levels of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) were evaluated by Real-time polymerase chain reaction (PCR) and Enzyme linked immunosorbent assay (ELISA). Results: Ang II caused sharply increase of the nuclear translocation of NF-κB p65, also, Ang II significantly increased expression of ICAM-1 and MCP-1 secreted by HASMCs, this effect could be inhibited by Ang-(1–7) and IRB. Conclusion: These data may indicate the effect of Ang II on inducing HASMCs to secret ICAM-1 and MCP-1, which might be through the NF-κB p65 pathway by AT-1 receptor.

Keywords

• human airway smooth muscle cells
• angiotensin II
• ICAM-1
• MCP-1
• NF-κB signal pathway