Caveolae, caveolin-1 and cavin-1: Emerging roles in pulmonary hypertension.
Caveolae, caveolin-1 and cavin-1: Emerging roles in pulmonary hypertension.
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DOI：
10.5320/wjr.v5.i2.126
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发表时间：
2015-07-28
期刊：
影响因子：
--
通讯作者：
Jin Y
中科院分区：
文献类型：
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作者：
Chettimada S;Yang J;Moon HG;Jin Y
小窝是细胞膜的瓶状内陷，起着重要的结构和功能作用。细胞膜小窝含有多种信号分子，用于跨膜接收、集中和传递细胞外信号。窖蛋白是存在于窖中的主要结构蛋白。Caveolins和另一类新发现的Caveolae调节蛋白cavins不仅负责Caveolae的形成，而且还与Caveolae中的信号复合物相互作用并调节信号的跨膜传递。在肺中，三种小窝蛋白同种型中的两种，即，cav-1和cav-2广泛表达。Cavin蛋白家族由4个蛋白组成，分别为cavin-1（PTRF，聚合酶Ⅰ和转录释放因子）、cavin-2（SDPR，血清剥夺蛋白反应）、cavin-3（SRBC，与c激酶结合的sdr相关基因产物）和cavin-4（MURC，肌肉限制性卷曲螺旋蛋白）。所有的小窝蛋白和cavin蛋白是小窝动力学的重要调节因子。近年来，研究表明小窝及其相关蛋白在肺动脉高压的发生、发展中起重要作用。本文就cav-1（cav-1）、cav-2和cavin-1（PTRF）在人肺动脉高压模型和实验性肺动脉高压模型中的表达变化及其下游信号传导机制作一综述。
Caveolae are flask-shaped invaginations of cell membrane that play a significant structural and functional role. Caveolae harbor a variety of signaling molecules and serve to receive, concentrate and transmit extracellular signals across the membrane. Caveolins are the main structural proteins residing in the caveolae. Caveolins and another category of newly identified caveolae regulatory proteins, named cavins, are not only responsible for caveolae formation, but also interact with signaling complexes in the caveolae and regulate transmission of signals across the membrane. In the lung, two of the three caveolin isoforms, i.e., cav-1 and -2, are expressed ubiquitously. Cavin protein family is composed of four proteins, named cavin-1 (or PTRF for polymerase Ⅰ and transcript release factor), cavin-2 (or SDPR for serum deprivation protein response), cavin-3 (or SRBC for sdr-related gene product that binds to-c-kinase) and cavin-4 (or MURC for muscle restricted coiled-coiled protein or cavin-4). All the caveolin and cavin proteins are essential regulators for caveolae dynamics. Recently, emerging evidence suggest that caveolae and its associated proteins play crucial roles in development and progression of pulmonary hypertension. The focus of this review is to outline and discuss the contrast in alteration of cav-1 (cav-1),-2 and cavin-1 (PTRF) expression and downstream signaling mechanisms between human and experimental models of pulmonary hypertension.