INTERLEUKIN-1-BETA ALTERS ACTIN EXPRESSION AND INHIBITS CONTRACTION OF RAT THORACIC AORTA

被引:10
|
作者
TRINKLE, LA
BEASLEY, D
MORELAND, RS
机构
[1] GRAD HOSP PHILADELPHIA,BOCKUS RES INST,415 S 19TH ST,PHILADELPHIA,PA 19146
[2] HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV RENAL,BOSTON,MA 02115
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1992年 / 262卷 / 04期
关键词
VASCULAR SMOOTH MUSCLE; PHOSPHORYLATION; MYOSIN LIGHT CHAIN; MYOSIN; ISOFORMS; PHENYLEPHRINE;
D O I
10.1152/ajpcell.1992.262.4.C828
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Previous studies have indicated that interleukin-1-beta (IL-1) inhibits contraction of rat aortas by activating nitric oxide production in vascular smooth muscle cells, with subsequent increases in guanosine 3',5'-cyclic monophosphate (cGMP). This study determined if the effect of IL-1 involves the primary regulatory event in smooth muscle activation, myosin light chain (MLC) phosphorylation. This study also examined whether IL-1 affects contractile protein content. IL-1 (20 ng/ml) significantly decreased stress in response to 0.1-mu-M phenylephrine with a concomitant decrease in MLC phosphorylation. Incubation with IL-1 for 3 h or longer decreased alpha-smooth muscle actin and increased gamma-actin isoform, with no change in beta-nonmuscle actin or myosin isozyme content. These results suggest that IL-1 inhibition of a vascular smooth muscle contraction may be due to a decrease in activator calcium, which may account for the resultant decrease in MLC phosphorylation. These results also indicate that IL-1 significantly affects contractile protein content, enhancing gamma-actin isoforms and decreasing the vascular smooth muscle specific alpha-isoactin.
引用
收藏
页码:C828 / C833
页数:6
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