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

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

DOI: 10.1016/j.preghy.2016.02.002

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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University of Melbourne Researchers

Tu'uhevaha Kaitu'u-Lino Author Obstetrics and Gynaecology Royal Women's Hospital/Mercy

Roxanne Hastie Author Obstetrics and Gynaecology Royal Women's Hospital/Mercy

Stephen Tong Author Obstetrics and Gynaecology Royal Women's Hospital/Mercy

Fiona Brownfoot Author Obstetrics and Gynaecology Royal Women's Hospital/Mercy

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Grants

Awarded by National Health and Medical Research Council of Australia

Funding Acknowledgements

The National Health and Medical Research Council of Australia provided salary (#1062418 to T.K., #1050765 to S.T.) and project support (#1048707). N.H. salary provided by CR Roper Fellowship and R.H. and F.B. via APA scholarships.