Journal article
Decreased STAT3 in human idiopathic fetal growth restriction contributes to trophoblast dysfunction
AJ Borg, HEJ Yong, M Lappas, SA Degrelle, RJ Keogh, F Da Silva-Costa, T Fournier, M Abumaree, JA Keelan, B Kalionis, P Murthi
Reproduction | BIOSCIENTIFICA LTD | Published : 2015
DOI: 10.1530/REP-14-0622
Abstract
Abnormal trophoblast function is associated with fetal growth restriction (FGR). The JAK-STAT pathway is one of the principal signalling mechanisms by which cytokines and growth factors modulate cell proliferation, differentiation, cell migration and apoptosis. The expression of placental JAK-STAT genes in human idiopathic FGR is unknown. In this study, we propose the hypothesis that JAK-STAT pathway genes are differentially expressed in idiopathic FGR-affected pregnancies and contribute to abnormal feto-placental growth by modulating the expression of the amino acid transporter SNAT2, differentiation marker CGB/human chorionic gonadotrophin beta-subunit (β-hCG) and apoptosis markers caspase..
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Awarded by Australian National Health and Medical Research Council
Funding Acknowledgements
This work was supported by The University of Melbourne Early Career Researcher Grant scheme, University of Melbourne Research Grant, University of Melbourne Research Fellowship and Australian National Health and Medical Research Council project grant number 509140 awarded to Dr P Murthi.