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1.
Basic & Clinical Medicine ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-588843

ABSTRACT

Objective To study whether focal adhesion kinase (FAK) promotes human pulmonary artery smooth cells (HPASMCs) proliferation.Methods Cultured HPASMCs stimulated by fibronectin (40 mg/L) were passively transfected with sense -FAK oligonucleotides(ODNs), FAK activity was measured by immunoprecipitation and expression of FAK protein was detected by Western blots.Meanwhile, the change of cell proliferation was measured by MTT and 3H-TdR absorbation experiment. Results The change of FAK activity and FAK protein content was dose and time dependent at diferential concentration and time passively transfected with sense-FAK ODNs in Cultured HPASMCs. At the same time, sense-FAK ODNs prompoted HPASMCs proliferation and 3H-TdR absorbation.Conclusion FAK can faciliate HPASMCs proliferation,which may play an important function in pulmonary artery hypertension development.

2.
Journal of Chinese Physician ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-527121

ABSTRACT

0.05).Conclusion The ET-1 promotes the expression of CDK_2 protein in HPASMCs,Which may play an important role in the proliferation of PASMCs.

3.
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-530015

ABSTRACT

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 G1 phase decreased significantly in FAK SODNs group,while the cells at S phase increased significantly.In contrast,the proportion of cells at G1 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.

4.
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-526879

ABSTRACT

AIM: To investigate whether focal adhesion kinase (FAK) takes part in the intracellular signaling pathway involved in apoptosis of human pulmonary artery smooth muscle cells (HPASMCs). METHODS: Cultured HPASMCs stimulated by fibronection (40 mg/L) were passively transfected with antisense-FAK oligodeoxynucleotides (ODNs). Expression of FAK and caspase-3 proteins was detected by immunoprecipitation and Western blotting. In addition, apoptosis were measured by TUNEL. RESULTS: The protein expression of FAK in HPASMCs decreased and caspase-3 expression upregulated in HPASMCs in antisense-FAK ODNs group. At the same time, antisense-FAK ODNs transfection increased the rate of cell apoptosis. CONCLUSION: These results suggest that FAK may be related with the apoptosis of HPASMCs. Antisense-FAK ODNs inhibit HPASMC proliferation and may facilitate their apoptosis via caspase-3 signaling pathway.

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