F-actin disruption attenuates agonist-induced [Ca2+], myosin phosphorylation, and force in smooth muscle

被引:53
作者
Tseng, S
Kim, R
Kim, T
Morgan, KG
Hai, CM
机构
[1] BROWN UNIV, DIV BIOL & MED, PROVIDENCE, RI 02912 USA
[2] HARVARD UNIV, SCH MED, BOSTON BIOMED RES INST, BOSTON, MA 02114 USA
[3] HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02114 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1997年 / 272卷 / 06期
关键词
asthma; calcium; cytoskeleton; receptor; signal transduction;
D O I
10.1152/ajpcell.1997.272.6.C1960
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cytochalasins B and D (at 10 mu M) inhibited stress development induced by 1 mu M carbachol in bovine tracheal smooth muscle by 55% and 90%, respectively. Glucose depletion was ineffective in inhibiting carbachol-induced contraction, indicating that inhibition of glucose transport was not the cause. Cytochalasin D-treated smooth muscle cells appeared collapsed, with spiky protrusions from the cell membrane. Deconvolution of fluorescent images of fluorescein isothiocyanate-phalloidin-labeled smooth muscle cells revealed concentrations of actin filaments near the cell periphery, including near the spiky protrusions. Cytochalasin B attenuated carbachol-induced intracellular Ca2+ concentration ([Ca2+]), especially the initial peak intracellular [Ca2+]. Cytochalasin B also attenuated carbachol-induced myosin light chain phosphorylation. However, when the myosin phosphorylation data were plotted against time-matched intracellular [Ca2+] data, the two relationships in control and cytochalasin B-treated smooth muscle were similar, suggesting that the changes in myosin phosphorylation could be explained by the changes in intracellular [Ca2+]. These results suggest that actin filaments in smooth muscle cells are dynamic and may be an integral component of Ca2+ regulation and/or signal transduction in receptor-coupled mechanisms.
引用
收藏
页码:C1960 / C1967
页数:8
相关论文
共 39 条
[1]   EFFECT OF CYTOCHALASIN-D ON SMOOTH-MUSCLE CONTRACTION [J].
ADLER, KB ;
KRILL, J ;
ALBERGHINI, TV ;
EVANS, JN .
CELL MOTILITY AND THE CYTOSKELETON, 1983, 3 (5-6) :545-551
[2]  
ALBERTS B, 1989, MOL BIOL CELL, P642
[3]   THE INVOLVEMENT OF THE CYTOSKELETON IN REGULATING IP(3) RECEPTOR-MEDIATED INTERNAL CA2+ RELEASE IN HUMAN BLOOD-PLATELETS [J].
BOURGUIGNON, LYW ;
IIDA, N ;
JIN, HT .
CELL BIOLOGY INTERNATIONAL, 1993, 17 (08) :751-758
[4]   ACTIN-FILAMENTS REGULATE EPITHELIAL NA+ CHANNEL ACTIVITY [J].
CANTIELLO, HF ;
STOW, JL ;
PRAT, AG ;
AUSIELLO, DA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (05) :C882-C888
[5]   INTEGRINS AND SIGNAL-TRANSDUCTION PATHWAYS - THE ROAD TAKEN [J].
CLARK, EA ;
BRUGGE, JS .
SCIENCE, 1995, 268 (5208) :233-239
[6]   EFFECTS OF CYTOCHALASIN AND PHALLOIDIN ON ACTIN [J].
COOPER, JA .
JOURNAL OF CELL BIOLOGY, 1987, 105 (04) :1473-1478
[7]   MUSCLE-CONTRACTION AND FREE-ENERGY TRANSDUCTION IN BIOLOGICAL-SYSTEMS [J].
EISENBERG, E ;
HILL, TL .
SCIENCE, 1985, 227 (4690) :999-1006
[8]   EFFECT OF CYTOCHALASIN-B ON THE METABOLISM OF POLYPHOSPHOINOSITIDES IN ADRENOCORTICAL-CELLS [J].
FEUILLOLEY, M ;
DESRUES, L ;
VAUDRY, H .
ENDOCRINOLOGY, 1993, 133 (05) :2319-2326
[9]   EFFECTS OF SELECTIVE DISRUPTION OF CYTOSKELETAL ELEMENTS ON STEROID-SECRETION BY HUMAN ADRENOCORTICAL SLICES [J].
FEUILLOLEY, M ;
CONTESSE, V ;
LEFEBVRE, H ;
DELARUE, C ;
VAUDRY, H .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (02) :E202-E210
[10]   AEQUORIN LUMINESCENCE, MYOSIN PHOSPHORYLATION, AND ACTIVE STRESS IN TRACHEAL SMOOTH-MUSCLE [J].
GERTHOFFER, WT ;
MURPHEY, KA ;
GUNST, SJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (06) :C1062-C1068