Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 311, Issue 6, Pages H1459-H1469Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00141.2016
Keywords
blood pressure; epigenetics; vitamin D; endothelial dysfunction; Pannexin-1
Funding
- Ubbo Emmius Fonds-Junior Scientific Masterclass (UEF-JSM)
- Netherlands Heart Foundation [2007T046]
- Innovational Research Incentives Scheme Program of the Netherlands Organization for Scientific Research (NWO VENI Grant) [916.10.117]
- Innovational Research Incentives Scheme Program of the Netherlands Organization for Scientific Research (NWO VIDI Grant) [917.13.350]
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Vitamin D deficiency is one of the most common nutritional deficiencies worldwide. Maternal vitamin D deficiency is associated with increased susceptibility to hypertension in offspring, but the reasons for this remain unknown. The aim of this study was to determine if parental vitamin D deficiency leads to altered DNA methylation in offspring that may relate to hypertension. Male and female Sprague-Dawley rats were fed a standard or vitamin D-depleted diet. After 10 wk, nonsibling rats were mated. The conceived pups received standard chow. We observed an increased systolic and diastolic blood pressure in the offspring from depleted parents (F1-depl). Genome-wide methylation analyses in offspring identified hypermethylation of the promoter region of the Pannexin-1 (Panx1) gene in F1-depl rats. Panx1 encodes a hemichannel known to be involved in endothelial-dependent relaxation, and we demonstrated that in F1-depl rats the increase in blood pressure was associated with impaired endothelial relaxation of the large vessels, suggesting an underlying biological mechanism of increased blood pressure in children from parents with vitamin deficiency. Parental vitamin D deficiency is associated with epigenetic changes and increased blood pressure levels in offspring.
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