Published online Jul 28, 2015. doi: 10.5320/wjr.v5.i2.126
Peer-review started: August 8, 2014
First decision: December 26, 2014
Revised: February 25, 2015
Accepted: June 15, 2015
Article in press: June 16, 2015
Published online: July 28, 2015
Processing time: 361 Days and 7.5 Hours
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.
Core tip: Pulmonary hypertension is a disease condition that is associated with a wide range of underlying medical conditions and environmental exposures. Currently, the exact molecular mechanisms underlying the pathogenesis of pulmonary hypertension remain unclear. This review is to outline and discuss the current understandings on the novel roles of a group of cell surface proteins, cav-1, -2 and cavin-1, on the development of pulmonary hypertension and vascular remodeling.