ArticleEndocrinology2012
Potassium channel mutant KCNJ5 T158A expression in HAC-15 cells increases aldosterone synthesis.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 170 citations in OpenAlex.
- Adrenal causes of endocrine hypertension in childhood or adolescence.Journal of endocrinological investigation · 2025Review
- Speculating suitability of partial adrenalectomy for lateralized primary aldosteronism: With emphasis on partial and complete success as optimistic outcomes.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- E3 ubiquitin ligase TRIM2 identified as a novel suppressor of CYP11B2 and aldosterone production.Cellular and molecular life sciences : CMLS · 2024Article
- mTOR Regulates Mineralocorticoid Receptor Transcriptional Activity by ULK1-Dependent and -Independent Mechanisms.Endocrinology · 2024Article
- Somatic SLC30A1 mutations altering zinc transporter ZnT1 cause aldosterone-producing adenomas and primary aldosteronism.Nature genetics · 2023Article
- Article
- 18-Oxocortisol: A journey.The Journal of steroid biochemistry and molecular biology · 2023Article
- Primary Aldosteronism: State-of-the-Art Review.American journal of hypertension · 2022Article
- Mammalian Target of Rapamycin Inhibition Decreases Angiotensin II-Induced Steroidogenesis in HAC15 Human Adrenocortical Carcinoma Cells.Endocrinology · 2022Article
- Hypomethylation associated vitamin D receptor expression in ATP1A1 mutant aldosterone-producing adenoma.Molecular and cellular endocrinology · 2022Article
- Genetics of Primary Aldosteronism.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Genetic Alterations in Benign Adrenal Tumors.Biomedicines · 2022Review
- Primary aldosteronism caused by a pI157S somaticFrontiers in endocrinology · 2022Article
- KCNJ5 Somatic Mutation Is Associated With Higher Aortic Wall Thickness and Less Calcification in Patients With Aldosterone-Producing Adenoma.Frontiers in endocrinology · 2022Article
- Aldosterone-Regulated Sodium Transport and Blood Pressure.Frontiers in physiology · 2022Review
- Article
- GENETICS IN ENDOCRINOLOGY: Impact of race and sex on genetic causes of aldosterone-producing adenomas.European journal of endocrinology · 2021Review
- Update on Genetics of Primary Aldosteronism.Biomedicines · 2021Review
- Effect of Dietary Sodium Modulation on Pig Adrenal Steroidogenesis and Transcriptome Profiles.Hypertension (Dallas, Tex. : 1979) · 2020Article
- The landscape of molecular mechanism for aldosterone production in aldosterone-producing adenoma.Endocrine journal · 2020Review
16 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Primary aldosteronism is the most common cause of secondary hypertension, most frequently due to an aldosterone-producing adenoma or idiopathic hyperaldosteronism. Somatic mutations of the potassium channel KCNJ5 in the region of the selectivity filter have been found in a significant number of aldosterone-producing adenomas. There are also familial forms of primary aldosteronism, one of which, familial hyperaldosteronism type 3 which to date has been found in one family who presented with a severe abnormality in aldosterone and 18-oxocortisol production and hypertrophy and hyperplasia of the transitional zone of the adrenal cortex. In familial hyperaldosteronism type 3, there is a genomic mutation causing a T158A change of amino acids within the selectivity filter region of the KCNJ5 gene. We are reporting our studies demonstrating that lentiviral-mediated expression of a gene carrying the T158A mutation of the KCNJ5 in the HAC15 adrenal cortical carcinoma cell line causes a 5.3-fold increase in aldosterone secretion in unstimulated HAC15-KCNJ5 cells and that forskolin-stimulated aldosterone secretion was greater than that of angiotensin II. Expression of the mutated KCNJ5 gene decreases plasma membrane polarization, allowing sodium and calcium influx into the cells. The calcium channel antagonist nifedipine and the calmodulin inhibitor W-7 variably inhibited the effect. Overexpression of the mutated KCNJ5 channel resulted in a modest decrease in HAC15 cell proliferation. These studies demonstrate that the T158A mutation of the KCNJ5 gene produces a marked stimulation in aldosterone biosynthesis that is dependent on membrane depolarization and sodium and calcium influx into the HAC15 adrenal cortical carcinoma cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.