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

Ning Li; Yating Huo; Haojun Xie; Yuanxiong Cheng

doi:10.3934/medsci.2018.3.259

AIMS Medical Science, 2018, 5(3): 259-267. doi: 10.3934/medsci.2018.3.259. Research article

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

Ning Li, Yating Huo, Haojun Xie, Yuanxiong Cheng

1 Department of Neurosurgery, The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China
2 Department of Respiratory Disease, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China

Received: , Accepted: , Published:

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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.

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Keywords: human airway smooth muscle cells; angiotensin II; ICAM-1; MCP-1; NF-κB signal pathway

Citation: Ning Li, Yating Huo, Haojun Xie, Yuanxiong Cheng. Angiotensin II induces the secretion of ICAM-1 and MCP-1 in human airway smooth muscle cells in vitro. AIMS Medical Science, 2018, 5(3): 259-267. doi: 10.3934/medsci.2018.3.259

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