Role of activin A in the pathogenesis of endothelial cell dysfunction in preeclampsia.
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.
['Hobson|Sebastian R|SR|', 'Acharya|Rutu|R|', 'Lim|Rebecca|R|', 'Chan|Siow Teng|ST|', 'Mockler|Joanne|J|', 'Wallace|Euan M|EM|']
D028341:Activins D000328:Adult D015415:Biomarkers D016022:Case-Control Studies D019332:Endothelin-1 D005260:Female D061307:Human Umbilical Vein Endothelial Cells D006801:Humans D018799:Intercellular Adhesion Molecule-1 D011225:Pre-Eclampsia D011247:Pregnancy D015854:Up-Regulation D019010:Vascular Cell Adhesion Molecule-1
Activin Preeclampsia Follistatin Endothelin ICAM VCAM