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Prenatal dexamethasone-induced programmed hypertension and renal programming

Jiunn-Ming Sheen1, Hong-Ren Yu1, Mao-Meng Tiao1

  • 1Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan.

Life Sciences
|April 30, 2015
PubMed

Insights

Prenatal dexamethasone (DEX) exposure in rats alters kidney gene expression, leading to programmed hypertension. Key genes in arachidonic acid metabolism and factors regulating blood pressure contribute to this condition.

Area of Science:

  • Developmental programming
  • Renal physiology
  • Endocrinology

Background:

  • Antenatal glucocorticoids can cause long-term health issues in offspring, including hypertension.
  • Prenatal dexamethasone (DEX) exposure is a known model for programmed hypertension.
  • The precise mechanisms of renal programming and DEX's impact on hypertension development are not fully understood.

Purpose of the Study:

  • To investigate the effects of prenatal DEX exposure on the renal transcriptome at different developmental stages.
  • To identify key genes and pathways involved in DEX-induced renal programming and hypertension.
  • To explore the relationship between DEX, programmed hypertension, and blood pressure regulatory factors.

Main Methods:

  • Pregnant rats were administered intraperitoneal dexamethasone (DEX) during late gestation (gestational days 16-22).
  • RNA next-generation sequencing (NGS) was used to analyze the renal transcriptome of male offspring.
  • Programmed hypertension in male offspring was assessed at 16 weeks of age.

Main Results:

  • Prenatal DEX consistently altered 431 renal transcripts from nephrogenesis through adulthood.
  • Differentially expressed genes related to blood pressure regulation were identified at pre-hypertensive (11 genes) and established hypertension (13 genes) stages.
  • Genes involved in arachidonic acid metabolism and endothelium-derived hyperpolarizing/contractile factors (EDHF/EDCF), such as Ephx2, were implicated.

Conclusions:

  • Prenatal DEX exposure disrupts the balance of EDHFs and EDCFs, potentially causing renal programming and hypertension.
  • The arachidonic acid metabolism pathway appears to be a significant contributor to programmed hypertension.
  • Identified genes and pathways offer potential therapeutic targets for preventing corticosteroid-induced programmed hypertension.
Abstract

Keywords:
Arachidonic acidEndothelium-derived contractile factorEndothelium-derived hyperpolarizing factorGlucocorticoidHypertensionNext-generation sequencing

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