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Aim: To investigate the effect of ERK signaling pathway on apoptosis of airway smooth muscle cells (ASMCs) in chronic asthmatic rats.
Methods: Thirty Wistar rats were assigned to two groups: control group (A group, n = 15)and chronic asthmatic group (B group, n = 15). The apoptosis of ASMCs were detected by Situ end labeling and Annexin-V FITC PI double staining. The expressions of bcl-2 and bax were detected by immunocytochemical staining. The levels of caspase-3 protein were detected by Western blot. ASMC were treated with ERK activator epidermal growth factor (EGF) and inhibitor PD98059.
Results: Compared with control group, the apoptotic index and the percentage of the early apoptotic cells in ASMC from chronic asthmatic group were significantly decreased. After treatment with PD98059, the apoptotic index, the percentage of the early apoptotic cells, the expression of bax and the expression of caspase-3 protein in ASMC from chronic asthmatic group were significantly increased, and the expression of bcl-2 in ASMC from chronic asthmatic group were significantly decreased. Compared with those before treatment, apoptotic index and the percentage of the early apoptotic cells were significantly increased in EGF-treated cells. PD98059 could markedly inhibit the effect of EGF.
Conclusion: Apoptotic activation is significantly decreased in ASMC from chronic asthmatic group while the endogenous proliferation activation is significantly increased. The regulation of cell apoptosis is possibly related to ERK signaling pathway. The bcl-2 family and caspase-3 may participate in the regulation mechanism of cell apoptosis by ERK signaling pathway in ASMC from chronic asthmatic group.
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