Mechanisms of angiotensin II- and arginine vasopressin-induced increases in protein synthesis and content in cultured rat aortic smooth muscle cells. Evidence for selective increases in smooth muscle isoactin expression.
Mechanisms of angiotensin II- and arginine vasopressin-induced increases in protein synthesis and content in cultured rat aortic smooth muscle cells. Evidence for selective increases in smooth muscle isoactin expression.
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血管紧张素 II 和精氨酸加压素诱导培养的大鼠主动脉平滑肌细胞中蛋白质合成和含量增加的机制。
DOI：
10.1161/01.res.68.1.288
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发表时间：
1991
影响因子：
20.1
通讯作者：
Owens,GK
中科院分区：
文献类型：
--
作者：
Turla,MB;Thompson,MM;Corjay,MH;Owens,GK
本实验室先前的研究已经证明，血管紧张素II（Ang II）和精氨酸加压素（AVP）是培养的大鼠主动脉平滑肌细胞的有效肥大剂。本研究确定了主要的蛋白质，积累在血管紧张素II诱导和AVP诱导的肥大细胞，并开始研究的机制，有助于他们的积累。血管紧张素II和/或AVP（1 μ M）诱导的平滑肌细胞肥大与许多细胞蛋白质含量的广泛增加有关，这些蛋白质通过一维和二维凝胶电泳解析。然而，增加在本质上也是选择性的，某些个别蛋白质的增加，包括肌动蛋白（2 - 3倍），波形蛋白（2.5- 7倍），原肌球蛋白（3 - 6倍）和肌球蛋白重链，远远超过细胞蛋白含量的总体增加（20-40%）。肌动蛋白含量的增加主要是由于平滑肌α-肌动蛋白的表达增加（3.6至7.5倍），而非肌肉β-肌动蛋白（1.7至2.5倍）。平滑肌α-肌动蛋白的增加伴随着平滑肌α-肌动蛋白mRNA的5倍至8倍的增加，表明这些变化不仅仅是由于翻译控制。结果表明，在培养的平滑肌细胞中，收缩激动剂诱导的肥大部分是由于平滑肌收缩蛋白的表达增加。此外，Ang II和AVP诱导平滑肌α-肌动蛋白选择性增加的事实表明，这些激动剂不仅可以调节血管平滑肌的生长，而且还可以促进血管平滑肌分化过程中平滑肌特异性收缩蛋白的表达。
Previous studies from this laboratory have demonstrated that angiotensin II (Ang II) and arginine vasopressin (AVP) are potent hypertrophic agents in cultured rat aortic smooth muscle cells. The present study identified major proteins that accumulate in Ang II-induced and AVP-induced hypertrophic cells and initiated studies of the mechanisms that contribute to their accumulation. Smooth muscle cell hypertrophy induced by Ang II and/or AVP (1 microM each) was associated with widespread increases in the content of many cellular proteins that were resolved by one- and two-dimensional gel electrophoresis. However, increases were also selective in nature, with increases in certain individual proteins, including actin (twofold to threefold), vimentin (2.5-fold to sevenfold), tropomyosin (threefold to sixfold), and myosin heavy chain, far exceeding overall increases in cellular protein content (20-40%). Increases in actin content were due largely to increased expression of smooth muscle alpha-actin (3.6- to 7.5-fold), as opposed to nonmuscle beta-actin (1.7- to 2.5-fold). Increases in smooth muscle alpha-actin were accompanied by a fivefold to eightfold increases in smooth muscle alpha-actin mRNA, indicating that these changes were not due exclusively to translational controls. Results demonstrate that contractile agonist-induced hypertrophy in cultured smooth muscle cells is due, in part, to increased expression of smooth muscle contractile proteins. Furthermore, the fact that Ang II and AVP induced selective increases in smooth muscle alpha-actin suggests that these agonists may not only regulate growth of vascular smooth muscle but may also promote expression of smooth muscle-specific contractile proteins during differentiation of vascular smooth muscle.