CDK and JNK mediate FAK to enhance proliferation in human pulmonary artery smooth cells

AIM:To find out the mechanism of focal adhesion kinase (FAK) facilitating human pulmonary artery smooth muscle cells (HPASMCs) proliferation.METHODS:HPASMCs were isolated from normal part of lungs of two carcinoma patients who undergone lung partial resection. Cultured HPASMCs stimulated by fibronection(40 mg/L) were passively transfected with ODNs, sense focal adhesion kinase (FAK), mismatch sense and antisense-FAK, respectively. Expression of FAK, Jun NH2-terminal kinase (JNK) and cyclin-dependent kinase2 (CDK2) proteins were detected by immunoprecipitation and Western blotting. Cell cycle and cell apoptosis were analyzed by flow cytometry. In addition, cytoplasma FAK expression was detected by immunohistochemistry staining.RESULTS:The protein expressions of FAK, JNK and CDK2 in HPASMCs decreased in FAK ASODNs group and increased in FAK SODNs group. Meanwhile, the proportion of cells at G1 phase decreased significantly in FAK SODNs group, while the cells at S phase increased significantly. In contrast, the proportion of cells at G1 phase was increased significantly in FAK ASODNs group. The level of cell apoptosis in FAK ASODNs group was higher. FAK expression in FAK SODNs group was strongly stained by immunocytochemistry, whereas that in FAK ASODNs group was weakly stained. CONCLUSION:The results suggest that FAK via JNK, CDK2 signaling pathway enhances HPASMCs proliferation.