Jiang Yong, Liu He, Liu Wen-Jing, Tong Hai-Bin, Chen Chang-Jun, Lin Fu-Gui, Zhuo Yan-Hang, Qian Xiao-Zhen, Wang Zeng-Bin, Wang Yu, Zhang Peng, Jia Hong-Liang
Medical Examination College, Jilin Medical University, People's Republic of China.
Life Science Research Center, Beihua University, Jilin, People's Republic of China.
Mol Cells. 2016 Apr 30;39(4):292-8. doi: 10.14348/molcells.2016.2223. Epub 2016 Feb 29.
Aquaporin 1 (AQP1) is expressed in most microvasculature endothelial cells and forms water channels that play major roles in a variety of physiologic processes. This study aimed to delineate the transcriptional regulation of AQP1 by Mef2c in endothelial cells. Mef2c cooperated with Sp1 to activate human AQP1 transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells (HUVEC). Over-expression of Mef2c, Sp1, or Mef2c/Sp1 increased HUVEC migration and tube-forming ability, which can be abolished AQP1 knockdown. These data indicate that AQP1 is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.
水通道蛋白1(AQP1)在大多数微血管内皮细胞中表达,并形成水通道,这些水通道在多种生理过程中起主要作用。本研究旨在阐明Mef2c在内皮细胞中对AQP1的转录调控作用。在人脐静脉内皮细胞(HUVEC)中,Mef2c与Sp1协同作用,通过结合人AQP1近端启动子来激活其转录。Mef2c、Sp1或Mef2c/Sp1的过表达增加了HUVEC的迁移和管形成能力,而AQP1基因敲低可消除这种能力。这些数据表明,AQP1是Mef2c调节内皮细胞血管生成和血管发生的直接靶点。