Inhibition of activin A signalling in a mouse model of pre-eclampsia

Lim R 1 , Adhikari S 2 , Gurusinghe S 2 , Leaw B 1 , Acharya R 2 , Rahman R 3 Show all authors , Ciayadi R 4 , Potdar M 4 , Kelso GF 4 , Hearn MT 4 , Wallace EM 5

Affiliations 

  • 1 The Ritchie Centre, MIMR-PHI Institute of Medical Research, Victoria, Australia; Department of Obstetrics and Gynaecology, Monash University, Victoria, Australia
  • 2 The Ritchie Centre, MIMR-PHI Institute of Medical Research, Victoria, Australia
  • 3 The Ritchie Centre, MIMR-PHI Institute of Medical Research, Victoria, Australia; UKM Medical Centre, Bandar Tun Razak, Kuala Lumpur, Malaysia
  • 4 Centre for Green Chemistry, Monash University, Victoria, Australia
  • 5 The Ritchie Centre, MIMR-PHI Institute of Medical Research, Victoria, Australia; Department of Obstetrics and Gynaecology, Monash University, Victoria, Australia. Electronic address: euan.wallace@monash.edu
Placenta, 2015 Aug;36(8):926-31.
PMID: 26138362 DOI: 10.1016/j.placenta.2015.06.004

Abstract

Pre-eclampsia remains a major cause of maternal and fetal morbidity and mortality. Despite intensive research over the last 50 years, significant therapeutic advances have yet to be realised. We recently reported on the role of activin A in the pathophysiology of pre-eclampsia, whereby a pre-eclampsia-like disease state was induced in pregnant mice through activin A infusion. Using the same animal model, the effects of inhibiting activin A signalling on this pre-eclampsia-like disease state have now been assessed with low molecular weight compounds structurally related to activin-receptor-like kinase (ALK) inhibitors.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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