Comparison between endocardial and great vessel endothelial cells: morphology, growth, and prostaglandin release.
Comparison between endocardial and great vessel endothelial cells: morphology, growth, and prostaglandin release.
复制标题
DOI：
10.1152/ajpheart.1995.268.1.h250
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
A. Mebazaa;R. Wetzel;M. Cherian;M. Abraham
中科院分区：
文献类型：
--
作者：
A. Mebazaa;R. Wetzel;M. Cherian;M. Abraham
血管（VEC）和心内膜内皮细胞（EEC）释放的血管活性介质尚未直接比较。在本研究中，比较了从同一动物采集的大血管（VEC；肺动脉和主动脉）和心内膜（EEC；右心室和左心室）培养的绵羊内皮细胞的体外形态和细胞生长特征以及前列腺素释放率。从形态上看，在烧瓶中，VEC 表现出经典的鹅卵石图案，而 EEC 则形成大量细胞质交叉和重叠。 EEC 的细胞增殖率高于 VEC (P < 0.05)：EEC 的倍增时间 (34 +/- 3 小时) 比 VEC (45 +/- 5 小时) 短。在静态（无流动）条件下，响应花生四烯酸和钙离子载体 A-23187，VEC 和 EEC 释放前列环素 (PGI2) 和前列腺素 E2 的速率没有不同。相反，响应流量和急性缺氧（O2 张力 = 35 Torr），EEC 中的 PGI2 释放速率高于 VEC（P < 0.0001）。灌注2小时后，正常氧条件下EEC的PGI2释放速率是VEC的19倍，缺氧条件下的PGI2释放速率是VEC的34倍。因此，我们的研究显示了 VEC 和 EEC 之间前列腺素释放的起源依赖性异质性的解剖位点。心内膜内皮比大血管内皮是 PGI2 的更多来源；在体内，心内膜内皮 PGI2 可能抑制局部血小板聚集并调节下游血管张力。
The release of vasoactive mediators by vascular (VEC) and endocardial endothelial cells (EEC) has not been directly compared. In this study, in vitro morphological and cell growth characteristics and the rate of prostanoid release were compared in cultured sheep endothelial cells from great vessels (VEC; pulmonary artery and aorta) and endocardium (EEC; right and left ventricles) harvested from the same animals. Morphologically, in flasks, VEC demonstrated the classic cobblestone pattern, whereas EEC developed numerous cytoplasmic interdigitations and overlaps. Rate of cell proliferation was greater for EEC than for VEC (P < 0.05): doubling time was shorter for EEC (34 +/- 3 h) than for VEC (45 +/- 5 h). Under static (no-flow) conditions, in response to arachidonic acid and calcium ionophore A-23187, the rate of prostacyclin (PGI2) and prostaglandin E2 release by VEC and EEC was not different. In contrast, in response to flow and acute hypoxia (O2 tension = 35 Torr), the rate of PGI2 release was greater in EEC than in VEC (P < 0.0001). After 2 h of perfusion, the rate of PGI2 release was 19-fold greater for EEC than for VEC during normoxia and 34-fold greater during hypoxia. Thus our study showed anatomic site of origin-dependent heterogeneity in prostanoid release between VEC and EEC. Endocardial endothelium is a greater source of PGI2 than great vessel endothelium; in vivo, endocardial endothelial PGI2 may inhibit local platelet aggregation and modulate downstream vascular tone.