Role of MAPK in the migration of human coronary artery smooth muscle cell into three-dimensional fibrin gel

• Published in: Zhongguo ying yong sheng li xue za zhi Vol. 21; no. 4; p. 388
• Main Authors: Han, Ya-Ling, Qi, Yan-Mei, Kang, Jian, Liang, Ming, Chen, Xing-Hua
• Format: Journal Article
• Language: Chinese
• Published: China 01.11.2005
• Subjects: Anthracenes - pharmacology; Cell Movement; Cells, Cultured; Coronary Vessels - cytology; Extracellular Signal-Regulated MAP Kinases - metabolism; Fibrin - metabolism; Flavonoids - pharmacology; Humans; Imidazoles - pharmacology; JNK Mitogen-Activated Protein Kinases - metabolism; MAP Kinase Signaling System; Muscle, Smooth, Vascular - cytology; Myocytes, Smooth Muscle - cytology; p38 Mitogen-Activated Protein Kinases - metabolism; Pyridines - pharmacology
• ISSN: 1000-6834

To investigate the role of MAPK in the migration of human coronary artery smooth muscle cells(HCASMC ) into three-dimensional fibrin gels. HCASMC were primarily cultured. HCASMC migration was measured with a phase-contrast microscope in the presence or absence of PD98059, SB203580, and SP600125, the inhibitors of ERK, p38, and JNK, respectively. Phosphorylation of ERK, p38 and JNK were analyzed by Western blotting in the presence or absence of PD98059, SB203580 or SP600125. HCASMC that migrated into the three-dimensional fibrin gel exhibited a characteristic elongated spindle-shaped appearance and formed vessel-like structure. The number of migrated HCASMC increased with incubation time and concentration of fibrinogen in the range between 0.8 g/L and 6.4 g/L. Western blot showed that fibrin induced phosphorylation of ERK, p38 and JNK time dependently and PD98059, SB203580 and SP600125 could inhibit their activation, respectively. Migration of HCASMC into the fibrin gels was inhibited by SP600125 20 micromol/L