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激活素A在子痫前期内皮细胞功能障碍发病机制中的作用。

Role of activin A in the pathogenesis of endothelial cell dysfunction in preeclampsia.

作者信息

Hobson Sebastian R, Acharya Rutu, Lim Rebecca, Chan Siow Teng, Mockler Joanne, Wallace Euan M

机构信息

Department of Obstetrics and Gynaecology, Monash University, 246 Clayton Road, Clayton, VIC 3168, Australia; The Ritchie Centre, Hudson Institute of Medical Research, Monash University, Clayton, VIC 3168, Australia; Monash Women's Services, Monash Health, Clayton, VIC 3168, Australia.

The Ritchie Centre, Hudson Institute of Medical Research, Monash University, Clayton, VIC 3168, Australia.

出版信息

Pregnancy Hypertens. 2016 Apr;6(2):130-3. doi: 10.1016/j.preghy.2016.03.001. Epub 2016 Mar 31.

Abstract

Circulating markers for endothelial activation such as endothelin-1 (ET-1), ICAM-1 and VCAM-1 are elevated in women with preeclampsia. Using human umbilical vein endothelial cells (HUVECs) as an in vitro model of the maternal vasculature, we show that activin A and preeclamptic serum upregulate ET-1, ICAM-1, and VCAM-1 in HUVECs. Further, we show that follistatin, a specific binding protein for activin, mitigates the upregulation of ET-1, ICAM-1 and VCAM-1 in HUVECs exposed to either activin A or preeclamptic serum. These data are consistent with activin A contributing to the pathophysiology of preeclampsia and suggest that therapies targeting activin signalling are worth exploring.

摘要

内皮素 -1(ET -1)、细胞间黏附分子 -1(ICAM -1)和血管细胞黏附分子 -1(VCAM -1)等内皮激活的循环标志物在子痫前期女性中升高。我们将人脐静脉内皮细胞(HUVECs)作为母体血管系统的体外模型,发现激活素A和子痫前期血清会上调HUVECs中的ET -1、ICAM -1和VCAM -1。此外,我们还发现,激活素的特异性结合蛋白卵泡抑素可减轻暴露于激活素A或子痫前期血清的HUVECs中ET -1、ICAM -1和VCAM -1的上调。这些数据与激活素A参与子痫前期的病理生理过程一致,并表明针对激活素信号传导的疗法值得探索。

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