Circulating endothelial cell number and viability are reduced by exposure to high altitude.

Patrizia Mancuso, Fedro Peccatori, Andrea Rocca, Angelica Calleri, Pierluigi Antoniotti, Cristina Rabascio, Luca Saronni, Laura Zorzino, Maria Teresa Sandri, Anna Zubani, Francesco Bertolini
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引用次数: 13

Abstract

High altitude and hypoxia are known to induce polycythemia, pulmonary hypertension, and vascular remodeling. The authors investigated a number of blood cell populations in 15 mountain trekkers before and after 12 days spent at >3000 m. Red blood cell and platelet count increased, whereas circulating hematopoietic stem cell (enumerated as CD34bright cells), circulating endothelial cell (CEC) and circulating endothelial progenitor (CEP) count significantly decreased. In particular, the authors observed a decrease in the count of viable CECs, and a decrease in the circulating levels of RNA of the endothelial-specific gene VE-cadherin, whereas the fraction of apoptotic/necrotic CECs was stable. These data suggest a unique pattern of modulation of surrogate markers of vascular remodeling induced by exposure to hypobaric hypoxia.

暴露在高海拔环境中会降低循环内皮细胞的数量和活力。
已知高海拔和低氧可诱发红细胞增多症、肺动脉高压和血管重构。作者调查了15名登山者在海拔>3000米12天之前和之后的一些血细胞数量。红细胞和血小板计数增加,而循环造血干细胞(列举为CD34bright细胞)、循环内皮细胞(CEC)和循环内皮祖细胞(CEP)计数明显减少。特别是,作者观察到存活的CECs数量减少,内皮特异性基因ve -钙粘蛋白的RNA循环水平下降,而凋亡/坏死CECs的比例保持稳定。这些数据表明,暴露于低气压缺氧诱导的血管重构替代标志物的调节的独特模式。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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