Increased migration in late G1 phase in cultured smooth muscle cells

被引:17
作者
Fukui, R
Amakawa, M
Hoshiga, M
Shibata, N
Kohbayashi, E
Seto, M
Sasaki, Y
Ueno, T
Negoro, N
Nakakoji, T
Ii, M
Nishiguchi, F
Ishihara, T
Ohsawa, N
机构
[1] Osaka Med Coll, Dept Internal Med 1, Takatsuki, Osaka 5698686, Japan
[2] Osaka Med Coll, Cent Res Lab, Takatsuki, Osaka 5698686, Japan
[3] Kaken Pharmaceut Co, Dev Res Labs, Dept Pharmacol, Yamashina Ku, Kyoto 607, Japan
[4] Asahi Chem Ind Co Ltd, Life Sci Res Inst, Lab Pharmacol Res 1, Fuji, Shizuoka 4160934, Japan
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2000年 / 279卷 / 04期
关键词
myosin; atherosclerosis;
D O I
10.1152/ajpcell.2000.279.4.C999
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Migration and proliferation of smooth muscle cells (SMC) contribute to neointimal formation after arterial injury. However, the relation between migration and proliferation in these cells is obscure. To discriminate between migration and proliferation, we employed a migration assay of SMC at different phases of the cell cycle. Serum-deprived SMC were synchronized in different phases of the cell cycle by addition of serum for various periods of time. Migration induced by platelet-derived growth factor B-chain homodimer was maximal in SMC that were predominantly in the late G(1) (G(1b)) phase. In addition, in nonsynchronized SMC, 65-75% of SMC that had migrated were in the G1b phase. Phosphorylated myosin light chain was enriched around the cell periphery in SMC in the G(1b) phase compared with SMC in the other cell cycle phases. Interestingly, the Triton X-100-insoluble fraction of myosin was remarkably decreased in G(1b)-enriched SMC. These findings suggest that migratory activity of SMC may be coupled with the G(1b) phase. The phosphorylation and retention of myosin might explain some of the properties responsible for increased migration.
引用
收藏
页码:C999 / C1007
页数:9
相关论文
共 46 条
[1]  
BALL RY, 1989, J CELL SCI, V93, P163
[2]   PHYLOGENETIC ANALYSIS OF THE MYOSIN SUPERFAMILY [J].
CHENEY, RE ;
RILEY, MA ;
MOOSEKER, MS .
CELL MOTILITY AND THE CYTOSKELETON, 1993, 24 (04) :215-223
[3]   SIGNIFICANCE OF QUIESCENT SMOOTH-MUSCLE MIGRATION IN THE INJURED RAT CAROTID-ARTERY [J].
CLOWES, AW ;
SCHWARTZ, SM .
CIRCULATION RESEARCH, 1985, 56 (01) :139-145
[4]   DISTINCTION BETWEEN 5-BROMODEOXYURIDINE LABELED AND UNLABELED MITOTIC CELLS BY FLOW-CYTOMETRY [J].
DARZYNKIEWICZ, Z ;
TRAGANOS, F ;
MELAMED, MR .
CYTOMETRY, 1983, 3 (05) :345-348
[5]   Myosin II transport, organization, and phosphorylation: Evidence for cortical flow solation-contraction coupling during cytokinesis and cell locomotion [J].
DeBiasio, RL ;
LaRocca, GM ;
Post, PL ;
Taylor, DL .
MOLECULAR BIOLOGY OF THE CELL, 1996, 7 (08) :1259-1282
[6]   THE DYNAMIC DISTRIBUTION OF FLUORESCENT ANALOGS OF ACTIN AND MYOSIN IN PROTRUSIONS AT THE LEADING-EDGE OF MIGRATING SWISS 3T3 FIBROBLASTS [J].
DEBIASIO, RL ;
WANG, LL ;
FISHER, GW ;
TAYLOR, DL .
JOURNAL OF CELL BIOLOGY, 1988, 107 (06) :2631-2645
[7]   3D ANALYSIS OF CELL-MOVEMENT DURING NORMAL AND MYOSIN-II-NULL CELL MORPHOGENESIS IN DICTYOSTELIUM [J].
DOOLITTLE, KW ;
REDDY, I ;
MCNALLY, JG .
DEVELOPMENTAL BIOLOGY, 1995, 167 (01) :118-129
[8]   INHIBITION OF NEOINTIMAL SMOOTH-MUSCLE ACCUMULATION AFTER ANGIOPLASTY BY AN ANTIBODY TO PDGF [J].
FERNS, GAA ;
RAINES, EW ;
SPRUGEL, KH ;
MOTANI, AS ;
REIDY, MA ;
ROSS, R .
SCIENCE, 1991, 253 (5024) :1129-1132
[9]   Inhibition of smooth muscle cell migration by the p21 cyclin-dependent kinase inhibitor (Cip1) [J].
Fukui, R ;
Shibata, N ;
Kohbayashi, E ;
Amakawa, M ;
Furutama, D ;
Hoshiga, M ;
Negoro, N ;
Nakakouji, T ;
Ii, M ;
Ishihara, T ;
Ohsawa, N .
ATHEROSCLEROSIS, 1997, 132 (01) :53-59
[10]   DENSITY OF MYOSIN-FILAMENTS IN THE RAT ANOCOCCYGEUS MUSCLE, AT REST AND IN CONTRACTION .2. [J].
GILLIS, JM ;
CAO, ML ;
GODFRAINDDEBECKER, A .
JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY, 1988, 9 (01) :18-29