Maternal AMPK pathway activation with uterine artery blood flow and fetal growth maintenance during hypoxia

Author:

Moore Lorna G.1ORCID,Lorca Ramón A.1ORCID,Gumina Diane L.12,Wesolowski Stephanie R.3ORCID,Reisz Julie A.4,Cioffi-Ragan Darleen25,Houck Julie A.16,Banerji Sarah1,Euser Anna G.5,D’Alessandro Angelo4,Hobbins John C.25,Julian Colleen G.67ORCID

Affiliation:

1. Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

2. The University of Colorado John C. Hobbins Perinatal Center, Denver, Colorado, United States

3. Division of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

4. Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

5. Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

6. Department of Biomedical Informatics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

7. Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

Abstract

Fetal growth restriction (FGR) is increased and uterine artery (UtA) blood flow is lower at high altitudes (HA) but not all HA pregnancies have FGR. Here we show that greater UtA diameter and blood flow at week 20 are positively correlated with higher expression of the gene encoding the α1-catalytic subunit of AMP protein kinase, PRKAA1, suggesting that increased AMPK activation may help to prevent the detrimental effects of chronic hypoxia on fetal growth.

Funder

HHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

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