Parental vitamin D deficiency during pregnancy is associated with increased blood pressure in offspring via<i>Panx1</i>hypermethylation

Meems, Laura M.G.; Mahmud, Hasan; Buikema, Hendrik; Tost, Jörg; Michel, Sven; Takens, Janny; Verkaik-Schakel, Rikst Nynke; Vreeswijk-Baudoin, Inge; Mateo-Leach, I. V.; Harst, Pim van der; Plösch, Torsten; Boer, Rudolf A. de

doi:10.1152/ajpheart.00141.2016

Cited by 41 publications

(18 citation statements)

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“…Pathways affected by such regulation include antigen processing and presentation, inflammation, regulation of cell death, cell proliferation, transmission of nerve impulse, neurogenesis, neuron differentiation, sensory organ development ( 105 ) and vitamin D metabolism ( 106 ). Vitamin D's epigenetic effects on genes involved in metabolism and immune function have been demonstrated in experimental animal models ( 107 , 108 ) and preliminary findings have been reported in humans ( 105 ). The effect of vitamin D status on total genomic changes cannot be ignored and represent one of the most exciting branches of research to be explored.…”

Section: Vitamin D-induced Genomic Alterations During Pregnancymentioning

confidence: 99%

The Implications of Vitamin D Status During Pregnancy on Mother and her Developing Child

2018

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Pregnancy is a time of tremendous growth and physiological changes for mother and her developing fetus with lifelong implications for the child. The concert of actions that must occur so mother does not reject the foreign tissue of the fetus is substantial. There must be exquisite balance between maternal tolerance to these foreign proteins of paternal origin but also immune surveillance and function such that the mother is not immunocompromised. When this process goes awry, the mother may experience such pregnancy complications as preeclampsia and infections. Vitamin D deficiency affects these processes. Controversy continues with regard to the optimal daily intake of vitamin D, when sunlight exposure should be taken into account, and how to define sufficiency during such vulnerable and critical periods of development. The importance of vitamin D supplementation during pregnancy in preventing some of the health risks to the mother and fetus appears linked to achieving 25(OH)D concentrations >40 ng/mL, the beginning point of the plateau where conversion of the vitamin D metabolite 25(OH)D, the pre-hormone, to 1,25(OH)2D, the active hormone, is optimized. Throughout pregnancy, the delivery of adequate vitamin D substrate—through sunlight or supplement—is required to protect both mother and fetus, and when in sufficient supply, favorably impacts the epigenome of the fetus, and in turn, long term health. There is a growing need for future research endeavors to focus not only on critical period(s) from pre-conception through pregnancy, but throughout life to prevent certain epigenetic changes that adversely affect health. There is urgency based on emerging research to correct deficiency and maintain optimal vitamin D status. The impact of vitamin D and its metabolites on genetic signaling during pregnancy in both mother and fetus is an area of great activity and still in its early stages. While vitamin D repletion during pregnancy minimizes the risk of certain adverse outcomes (e.g., preterm birth, asthma, preeclampsia, and gestational diabetes), the mechanisms of how these processes occur are not fully understood. As we intensify our research efforts in these areas. it is only a matter of time that such mechanisms will be defined.

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Section: Vitamin D-induced Genomic Alterations During Pregnancymentioning

confidence: 99%

The Implications of Vitamin D Status During Pregnancy on Mother and her Developing Child

2018

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“…For instance, in a number of studies hypertension developed as a consequence of VDD, whereas the blood pressure remained unaltered in other studies (Table 2). According to the literature, VDD during the prenatal period leads to increased blood pressure in rodents' offsprings [25][26][27][28][29] probably due to the upregulation of the renin-angiotensin system [18,30]. Interestingly, VDD in utero contributes to the development of hypertension in later life even if the offsprings were fed with VitD sufficient chow after weaning [25,26], which implies that VDD during pregnancy can severely impact the offspring's long-term health and lead to vulnerability to cardiovascular disease in adult life [18,31].…”

Section: Discussionmentioning

confidence: 99%

“…According to the literature, VDD during the prenatal period leads to increased blood pressure in rodents' offsprings [25][26][27][28][29] probably due to the upregulation of the renin-angiotensin system [18,30]. Interestingly, VDD in utero contributes to the development of hypertension in later life even if the offsprings were fed with VitD sufficient chow after weaning [25,26], which implies that VDD during pregnancy can severely impact the offspring's long-term health and lead to vulnerability to cardiovascular disease in adult life [18,31]. However, when VDD affects only the postnatal period of life, the observations are controversial both in growing and adult rodents; nevertheless longer exposure to VDD appears to increase the risk of manifestation of hypertension [25,[32][33][34][35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, VDD in utero contributes to the development of hypertension in later life even if the offsprings were fed with VitD sufficient chow after weaning [25,26], which implies that VDD during pregnancy can severely impact the offspring's long-term health and lead to vulnerability to cardiovascular disease in adult life [18,31]. However, when VDD affects only the postnatal period of life, the observations are controversial both in growing and adult rodents; nevertheless longer exposure to VDD appears to increase the risk of manifestation of hypertension [25,[32][33][34][35][36][37][38]. Taken together, the development of hypertension appears to depend on the time of onset and the duration of VDD (Table 2).…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Deficiency Causes Inward Hypertrophic Remodeling and Alters Vascular Reactivity of Rat Cerebral Arterioles

Pál

Hadjadj

Fontányi

et al. 2018

Journal of Hypertension

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Background and purpose Vitamin D deficiency (VDD) is a global health problem, which can lead to several pathophysiological consequences including cardiovascular diseases. Its impact on the cerebrovascular system is not well understood. The goal of the present work was to examine the effects of VDD on the morphological, biomechanical and functional properties of cerebral arterioles. Methods Four-week-old male Wistar rats (n = 11 per group) were either fed with vitamin D deficient diet or received conventional rat chow with per os vitamin D supplementation. Cardiovascular parameters and hormone levels (testosterone, androstenedione, progesterone and 25hydroxyvitamin D) were measured during the study. After 8 weeks of treatment anterior cerebral artery segments were prepared and their morphological, biomechanical and functional properties were examined using pressure microangiometry. Resorcin-fuchsin and smooth muscle actin staining were used to detect elastic fiber density and smooth muscle cell counts in the vessel wall, respectively. Sections were immunostained for eNOS and COX-2 as well. Results VDD markedly increased the wall thickness, the wall-to-lumen ratio and the wall cross-sectional area of arterioles as well as the number of smooth muscle cells in the tunica media. As a consequence, tangential wall stress was significantly lower in the VDD group. In addition, VDD increased the myogenic as well as the uridine 5'-triphosphate-induced tone and impaired bradykinin-induced relaxation. Decreased eNOS and increased COX-2 expression were also observed in the endothelium of VDD animals.

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“…Interestingly, Meems et al discovered that vitamin D-deficient parental rats had offspring with increased systolic and diastolic BPs ( 67 ). The offspring were found to have hypermethylation of the promoter region of the Panx1 gene.…”

Section: Epigenetics Of Htnmentioning

confidence: 99%

Genetic Programming of Hypertension

Ahn

Gupta

2018

Front. Pediatr.

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The heritability of hypertension (HTN) is widely recognized and as a result, extensive studies ranging from genetic linkage analyses to genome-wide association studies are actively ongoing to elucidate the etiology of both monogenic and polygenic forms of HTN. Due to the complex nature of essential HTN, however, single genes affecting blood pressure (BP) variability remain difficult to isolate and identify and have rendered the development of single-gene targeted therapies challenging. The roles of other causative factors in modulating BP, such as gene–environment interactions and epigenetic factors, are increasingly being brought to the forefront. In this review, we discuss the various monogenic HTN syndromes and corresponding pathophysiologic mechanisms, the different methodologies employed in genetic studies of essential HTN, the mechanisms for epigenetic modulation of essential HTN, pharmacogenomics and HTN, and finally, recent advances in genetic studies of essential HTN in the pediatric population.

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Parental vitamin D deficiency during pregnancy is associated with increased blood pressure in offspring viaPanx1hypermethylation

Cited by 41 publications

References 55 publications

The Implications of Vitamin D Status During Pregnancy on Mother and her Developing Child

The Implications of Vitamin D Status During Pregnancy on Mother and her Developing Child

Vitamin D Deficiency Causes Inward Hypertrophic Remodeling and Alters Vascular Reactivity of Rat Cerebral Arterioles

Genetic Programming of Hypertension

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