Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension

被引:106
作者
Gao, Yuansheng [1 ]
Chen, Tianji [2 ]
Raj, J. Usha [2 ]
机构
[1] Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr, Beijing 100871, Peoples R China
[2] Univ Illinois, Coll Med, Dept Pediat, Chicago, IL USA
基金
中国国家自然科学基金;
关键词
paracrine; myoendothelial injunction; microvesicles; vasoconstriction; vascular remodeling; SOLUBLE GUANYLATE-CYCLASE; DEPENDENT PROTEIN-KINASE; MYOENDOTHELIAL GAP-JUNCTIONS; RECEPTOR GENE-EXPRESSION; NITRIC-OXIDE SYNTHASE; HIGH-ALTITUDE HYPOXIA; ARTERIAL-HYPERTENSION; EXTRACELLULAR VESICLES; OXIDATIVE-STRESS; NADPH OXIDASE;
D O I
10.1165/rcmb.2015-0323TR
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the pulmonary vasculature, the endothelial and smooth muscle cells are two key cell types that play a major role in the pathobiology of pulmonary vascular disease and pulmonary hypertension. The normal interactions between these two cell types are important for the homeostasis of the pulmonary circulation, and any aberrant interaction between them may lead to various disease states including pulmonary vascular remodeling and pulmonary hypertension. It is well recognized that the endothelial cell can regulate the function of the underlying smooth muscle cell by releasing various bioactive agents such as nitric oxide and endothelin-1. In addition to such paracrine regulation, other mechanisms exist by which there is cross-talk between these two cell types, including communication via the myoendothelial injunctions and information transfer via extracellular vesicles. Emerging evidence suggests that these nonparacrine mechanisms play an important role in the regulation of pulmonary vascular tone and the determination of cell phenotype and that they are critically involved in the pathobiology of pulmonary hypertension.
引用
收藏
页码:451 / 460
页数:10
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