期刊
BIOMEDICINES
卷 9, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines9050567
关键词
immunohistochemistry; adrenal cortex; aldosterone; cellular senescence
资金
- Ministry of Health, Labour, and Welfare, Japan [H29-Nanji-Ippan-046]
The study revealed that in aldosterone-producing adenomas and idiopathic hyperaldosteronism, cells in the zona glomerulosa exhibited significantly higher levels of senescence compared to other regions. Additionally, laboratory findings of primary aldosteronism were significantly correlated with specific gene mutations.
In situ cortisol excess was previously reported to promote cellular senescence, a cell response to stress, in cortisol-producing adenomas (CPA). The aim of this study was to explore senescence pathways in aldosterone-producing cells and related disorders, and the influence of aldosterone overproduction on in situ senescence. We analyzed 30 surgical cases of aldosterone-producing adenoma (APA), 10 idiopathic hyperaldosteronism (IHA) and 19 normal adrenals (NA). CYP11B2 and senescence markers p16 and p21 were immunolocalized in all those cases above and results were correlated with histological/endocrinological findings. In the three cohorts examined, the zona glomerulosa (ZG) was significantly more senescent than other corticosteroid-producing cells. In addition, the ZG of adjacent non-pathological adrenal glands of APA and IHA had significantly higher p16 expression than adjacent non-pathological zona fasciculata (ZF), reticularis (ZR) and ZG of NA. In addition, laboratory findings of primary aldosteronism (PA) were significantly correlated with p21 status in KCNJ5-mutated tumors. Results of our present study firstly demonstrated that non-aldosterone-producing cells in the ZG were the most senescent compared to other cortical zones and aldosterone-producing cells in PA. Therefore, aldosterone production, whether physiological or pathological, could be maintained by suppression of cell senescence in human adrenal cortex.
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