Journal article

Loss of Akt increases soluble endoglin release from endothelial cells but not placenta

Tu'uhevaha J Kaitu'u-Lino, Roxanne Hastie, Natalie J Hannan, Fiona Brownfoot, Manarangi De Silva, Ping Cannon, Laura Tuohey, Stephen Tong

PREGNANCY HYPERTENSION-AN INTERNATIONAL JOURNAL OF WOMENS CARDIOVASCULAR HEALTH | ELSEVIER SCI LTD | Published : 2016

Abstract

INTRODUCTION: Preeclampsia is a serious pregnancy complication for which there are no medical treatments. Soluble endoglin is an anti-angiogenic factor implicated in the pathogenesis of the disease, however little is known about its molecular regulation. The PI3K/Akt pathway is down regulated in preeclamptic placentas and decreased PI3K/Akt signaling has been linked to increased soluble endoglin release from endothelial cells. MMP14 is a key protease that functions to release soluble endoglin from the placental surface. OBJECTIVE: This study aimed to determine whether reduced placental PI3K/Akt causes elevated release of soluble endoglin via MMP14. STUDY DESIGN: Akt mRNA and protein expressi..

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