Ask about this productRelated genes to: CYP11B2 Blocking Peptide
- Gene:
- CYP11B2 NIH gene
- Name:
- cytochrome P450 family 11 subfamily B member 2
- Previous symbol:
- CYP11B
- Synonyms:
- CYP11BL, CPN2, P-450C18, P450aldo, ALDOS
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: CYP11B2 Blocking Peptide
Related articles to: CYP11B2 Blocking Peptide
- Metabolic reprogramming is increasingly recognized as a key driver of endocrine tumor biology, yet how dysregulated metabolism promotes aldosterone excess in aldosterone-producing adenomas remains largely unclear. - Source: PubMed
Publication date: 2026/06/04
Sun MinGao MaotingLiu YuqingXia ZhiqingMa LinqiangShi NaipengZhang YongjieSun ShanliangTao JunBao MeilingZhou MeiWang CongYang TaoZhang ZhihengYang Yuhong - The placenta produces a variety of steroid hormones through the catalytic activity of steroidogenic enzymes, including cytochrome P450 (CYP) hydroxylases and hydroxysteroid dehydrogenases (HSD). Large amounts of progesterone produced by the placenta are essential for the maintenance of pregnancy. Although androgens and estrogens are also elevated in maternal circulation during gestation, there are conflicting reports on whether de novo synthesis of these steroids occurs in the human placenta. To address this issue, we performed a comprehensive analysis of steroidogenic gene expression in early and term placenta. While none of the genes examined showed binary expression changes, 17β-HSDs, including HSD17B1 and AKR1C3, were markedly upregulated in the term placenta. CYP19A1 and HSD11B2 genes were also markedly upregulated. In contrast, CYP17A1, CYP21A2, CYP11B1, CYP11B2, and HSD17B3 were almost undetectable. Consistent with these findings, the plasma ratios of active to precursor sex steroids (estradiol/estrone and testosterone/androstenedione) were higher in pregnant than in non-pregnant women, although concentrations of all steroids increased. In contrast, plasma levels and profiles of 11-oxygenated androgens were unchanged. These results indicate that the human placenta does not significantly contribute to circulating levels of either classical or novel classes of androgens. Therefore, this study provides new insights into the tissue of origin and the physiological significance of sex steroids during gestation. - Source: PubMed
Publication date: 2026/05/12
Yokohama YukoWatanabe YugoNakajima Ke-IchiUmezawa AkihiroTakahashi SatoruMori YasuhiroKato YasuhitoKawabe Jun-IchiYazawa Takashi - The mouse adrenal gland is encapsulated by a mesenchymal cell layer (capsule) and contains an underlying cortex organized into distinct concentric zones with specialized endocrine functions: the zona glomerulosa (zG), which produces aldosterone, and the zona fasciculata (zF), which produces corticosterone. The adrenal medulla, located at the center of the gland, produces catecholamines. Mechanistic studies of cells from each adrenocortical zone have been limited by the absence of in vitro models that preserve their zone-specific molecular, cellular, and functional characteristics. To overcome this limitation, a fractionation approach was developed using microdissection of adult mouse adrenal glands. This method separates adrenal cells from male mice into a zG-enriched outer fraction (OF), containing capsule and zG cells, and a zF-enriched inner fraction (IF), which contains zF and medullary cells. These fractions were used to generate two-dimensional (2D) primary cultures enriched for either zG or zF cells. Gene expression analysis confirmed that the zG-enriched cultures express high levels of zG markers (Cyp11b2, Dab2, and Shh), along with increased Wnt/β-catenin pathway markers (Wnt4, Lef1). In contrast, zF-enriched cultures exhibited higher expression of zF markers (Cyp11b1 and Akr1b7) and lower levels of Wnt/β-catenin pathway markers, consistent with a zF transcriptional signature. Expression of steroidogenic markers (Nr5a1, Star) validated the adrenocortical origin of both cell fractions. Tyrosine hydroxylase indicates the presence of adrenal medullary cells in zF-enriched cultures. Functionally, zG-enriched cultures produced aldosterone under basal conditions and showed increased production in response to angiotensin II, potassium, and adrenocorticotropic hormone (ACTH). Conversely, zF-enriched cultures produced corticosterone at baseline and exhibited increased output in response to ACTH stimulation. Overall, this protocol represents a robust, reproducible, and biologically relevant in vitro model for studying adrenal cortex biology. This system enables zone-specific investigation of signaling pathways, molecular mechanisms, and physiological responses. - Source: PubMed
Publication date: 2026/05/08
Kremer Jean LucasBorges Kleiton SilvaRibeiro ClaudioBerber MesutHaykir BetulCarlone Diana LLotfi Claudimara Ferini PaciccoBreault David T - In adrenal venous sampling (AVS) for patients with primary aldosteronism (PA), apparent bilateral aldosterone suppression (ABAS) is occasionally experienced, but the underlying causes remain poorly understood. - Source: PubMed
Publication date: 2026/06/01
Pan XiaoxiMa YuKang YuanyuanGao PingjinXu Jianzhong - We describe histopathological and ultrastructural evidence of osilodrostat-induced regression of a cortisol- and possibly aldosterone-producing adrenocortical adenoma. An 82-year-old woman with adrenal Cushing syndrome received preoperative osilodrostat therapy. Seventy days after starting osilodrostat, the patient developed an adrenal crisis, and the adrenal tumor obviously decreased in size. Laparoscopic adrenalectomy was performed 11 months after osilodrostat plus hydrocortisone treatment. Histological examination revealed no evident hemorrhage, necrosis, or conspicuous apoptosis. Instead, diffuse and extensive infiltration of CD163-positive histiocytes was observed, outnumbering the tumor cells. Residual neoplastic cells exhibited a global reduction in the expression of cortisol-synthesizing enzymes. Notably, focal weak CYP11B2 (aldosterone synthase) positivity was detected in the tumor, whereas adjacent nontumorous cortex showed preserved rather prominent CYP11B2 expression. Electron microscopy showed a marked loss of organelles essential for steroidogenesis. These findings suggest that osilodrostat exerts biochemical suppression of both cortisol and aldosterone secretion and modulates the morphology and function of the adrenocortical adenoma tissue. - Source: PubMed
Publication date: 2026/05/18
Kanzawa MakiMaeda TakeshiOhta YoshioOhno YasuhiroNakamura YasuhiroChihara Kazuo