ArticleMolecular and cellular endocrinology2014
Aberrant gonadotropin-releasing hormone receptor (GnRHR) expression and its regulation of CYP11B2 expression and aldosterone production in adrenal aldosterone-producing adenoma (APA).
Article in Molecular and cellular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- The adrenal gland and primary aldosteronism: anatomy, steroidogenesis, regulation, and genetic insights.Frontiers in endocrinology · 2025Review
- GENETICS IN ENDOCRINOLOGY: Impact of race and sex on genetic causes of aldosterone-producing adenomas.European journal of endocrinology · 2021Review
- MiR-193a-3p functions as a tumour suppressor in human aldosterone-producing adrenocortical adenoma by down-regulating CYP11B2.International journal of experimental pathology · 2018Article
- The prevalence of CTNNB1 mutations in primary aldosteronism and consequences for clinical outcomes.Scientific reports · 2017Article
- Gonadotropin-Releasing Hormone Stimulate Aldosterone Production in a Subset of Aldosterone-Producing Adenoma.Medicine · 2016Article
- Pregnancy, Primary Aldosteronism, and Adrenal CTNNB1 Mutations.The New England journal of medicine · 2015Article
- Understanding primary aldosteronism: impact of next generation sequencing and expression profiling.Molecular and cellular endocrinology · 2015Review
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Authors and funding
11 authors at 4 institutions in 3 countries.
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Abstract
Aberrant expression of gonadotropin-releasing hormone receptor (GnRHR) has been reported in human adrenal tissues including aldosterone-producing adenoma (APA). However, the details of its expression and functional role in adrenals are still not clear. In this study, quantitative RT-PCR analysis revealed the mean level of GnRHR mRNA was significantly higher in APAs than in human normal adrenal (NA) (P=0.004). GnRHR protein expression was detected in human NA and neoplastic adrenal tissues. In H295R cells transfected with GnRHR, treatment with GnRH resulted in a concentration-dependent increase in CYP11B2 reporter activity. Chronic activation of GnRHR with GnRH (100nM), in a cell line with doxycycline-inducible GnRHR (H295R-TR/GnRHR), increased CYP11B2 expression and aldosterone production. These agonistic effects were inhibited by blockers for the calcium signaling pathway, KN93 and calmidazolium. These results suggest GnRH, through heterotopic expression of its receptor, may be a potential regulator of CYP11B2 expression levels in some cases of APA.
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