Physical activity differentially regulates VEGF, PlGF, and their receptors in the human placenta
Open Access
- 19 January 2021
- journal article
- research article
- Published by Wiley in Physiological Reports
- Vol. 9 (2), e14710
- https://doi.org/10.14814/phy2.14710
Abstract
Physical activity (PA) has beneficial effects on the function of many organs by modulating their vascular development. Regular PA during pregnancy is associated with favorable short‐ and long‐term outcomes for both mother and fetus. During pregnancy, appropriate vascularization of the placenta is crucial for adequate maternal–fetal nutrient and gas exchange. How PA modulates angiogenic factors, VEGF, and its receptors in the human placenta, is as of yet, unknown. We objectively measured the PA of women at 24–28 and 34–38 weeks of gestation. Participants were considered “active” if they had met or exceeded 150 min of moderate‐intensity PA per week during their 2nd trimester. Term placenta tissues were collected from active (n = 23) or inactive (n = 22) women immediately after delivery. We examined the expression of the angiogenic factors VEGF, PlGF, VEGFR‐1, and VEGFR‐2 in the placenta. Western blot analysis showed VEGF and its receptor, VEGFR‐1 was significantly (p < 0.05) higher both at the protein and mRNA levels in placenta from physically active compared to inactive women. No difference in VEGFR‐2 was observed. Furthermore, immunohistochemistry showed differential staining patterns of VEGF and its receptors in placental endothelial, stromal, and trophoblast cells and in the syncytial brush border. In comparison, PlGF expression did not differ either at the protein or mRNA level in the placenta from physically active or inactive women. The expression and localization pattern of VEGF and its receptors suggest that PA during pregnancy may support a pro‐angiogenic milieu to the placental vascular network.Funding Information
- Canadian Institutes of Health Research (MOP 142298)
- Natural Sciences and Engineering Research Council of Canada (RGPIN‐2017‐05457)
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