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

TJ Kaitu'u-Lino; R Hastie; NJ Hannan; F Brownfoot; M De Silva; P Cannon; L Tuohey; S Tong

Journal article

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

TJ Kaitu'u-Lino, R Hastie, NJ Hannan, F Brownfoot, M De Silva, P Cannon, L Tuohey, S Tong

Pregnancy Hypertension | 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 expression ..

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University of Melbourne Researchers

Tu'uhevaha Kaitu'u-Lino Author

Natalie Hannan Author

Fiona Brownfoot Author

Ping Cannon Author

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Grants

Awarded by National Health and Medical Research Council

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.