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前列环素合酶的过表达抑制血管平滑肌细胞的生长。

Overexpression of prostacyclin synthase inhibits growth of vascular smooth muscle cells.

作者信息

Hara S, Morishita R, Tone Y, Yokoyama C, Inoue H, Kaneda Y, Ogihara T, Tanabe T

机构信息

Department of Pharmacology, Osaka University Medical School, Japan.

出版信息

Biochem Biophys Res Commun. 1995 Nov 22;216(3):862-7. doi: 10.1006/bbrc.1995.2701.

DOI:10.1006/bbrc.1995.2701
PMID:7488205
Abstract

To define the local effects of prostacyclin (PGI2) on the growth of vascular smooth muscle cells (VSMC), we transfected VSMC with an expression vector harboring the cDNA for PGI2 synthase (PGIS), which catalyzes the rearrangement of prostaglandin H2 to PGI2. Transfection of the human PGIS cDNA into rat VSMC did not affect DNA synthesis under serum-free basal conditions, but it increased PGI2 synthesis and decreased DNA synthesis under serum-stimulated conditions (in the presence of 1 or 5% fetal calf serum). These results demonstrated that locally synthesized PGI2 can exert autocrine and/or paracrine inhibitory effects on VSMC growth. It was also suggested that in vivo transfer of PGIS gene may be useful for the gene therapy for vascular disease such as neointimal hyperplasia.

摘要

为了确定前列环素(PGI2)对血管平滑肌细胞(VSMC)生长的局部作用,我们用携带PGI2合成酶(PGIS)cDNA的表达载体转染VSMC,PGIS催化前列腺素H2重排为PGI2。将人PGIS cDNA转染到大鼠VSMC中,在无血清基础条件下不影响DNA合成,但在血清刺激条件下(存在1%或5%胎牛血清)可增加PGI2合成并减少DNA合成。这些结果表明,局部合成的PGI2可对VSMC生长发挥自分泌和/或旁分泌抑制作用。还提示PGIS基因的体内转移可能对诸如内膜增生等血管疾病的基因治疗有用。

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Overexpression of prostacyclin synthase inhibits growth of vascular smooth muscle cells.前列环素合酶的过表达抑制血管平滑肌细胞的生长。
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