ArticleReproductive sciences (Thousand Oaks, Calif.)2011
Long-term hypoxia enhances cortisol biosynthesis in near-term ovine fetal adrenal cortical cells.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Methods of collection, extender type, and freezability of semen collected from creole bulls raised in the tropical highlands of Ecuador.Tropical animal health and production · 2019Article
- Preeclampsia link to gestational hypoxia.Journal of developmental origins of health and disease · 2019Review
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Expression of StAR and Key Genes Regulating Cortisol Biosynthesis in Near Term Ovine Fetal Adrenocortical Cells: Effects of Long-Term Hypoxia.Reproductive sciences (Thousand Oaks, Calif.) · 2018Article
- Adrenocorticotropic Hormone and PI3K/Akt Inhibition Reduce eNOS Phosphorylation and Increase Cortisol Biosynthesis in Long-Term Hypoxic Ovine Fetal Adrenal Cortical Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2015Article
- Extracellular signal-regulated kinases (ERK1/2) signaling pathway plays a role in cortisol secretion in the long-term hypoxic ovine fetal adrenal near term.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Leptin receptor antagonist treatment ameliorates the effects of long-term maternal hypoxia on adrenal expression of key steroidogenic genes in the ovine fetus.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Adrenocortical and adipose responses to high-altitude-induced, long-term hypoxia in the ovine fetus.Journal of pregnancy · 2012Review
- Nitric oxide inhibits ACTH-induced cortisol production in near-term, long-term hypoxic ovine fetal adrenocortical cells.Reproductive sciences (Thousand Oaks, Calif.) · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
This study was designed to determine the potential mechanism/mechanisms of previously observed enhanced fetal cortisol secretion following exposure to long-term hypoxia (LTH). Pregnant ewes were maintained at high altitude (3820 m) for approximately the last 100 days of gestation. Between the gestation days of 138 and 141, adrenal glands were collected from LTH and age-matched normoxic control fetuses. Cyclic adenosine monophosphate (cAMP), cortisol, and steroidogenic acute regulatory (StAR) protein were measured in response to adrenocorticotropic hormone (ACTH) stimulation. Cortisol responses to ACTH were also measured in the presence of the protein kinase (PKA) inhibitor H-89, proopiomelanocortin (POMC), or 22-kDa pro-ACTH. Cortisol output was higher in the LTH group compared to the control (P < .05), following ACTH treatment while the cAMP response was similar in both groups. Although PKA inhibition decreased cortisol production in both groups, however no differences were observed between groups. Western analysis revealed a significant increase in protein expression for StAR in the LTH group (P < .05, compared to control). Proopiomelanocortin and 22-kDa pro-ACTH did not alter the cortisol response to ACTH treatment. Results from the present study taken together with those of previous in vivo studies suggest that the enhanced cortisol output in the LTH group is not the result of differences in cAMP generation or PKA. We conclude that enhanced cortisol production in LTH adrenals is the result of enhanced protein expression of StAR and potential downstream signaling pathways.
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