Role of Mast Cells in the Control of Aldosterone
                    Secretion

Lopez, Antoine-Guy; Duparc, Céline; Naccache, Alexandre; Castanet, Mireille; Lefebvre, Henri; Louiset, Estelle

doi:10.1055/a-1119-1063

Cited by 12 publications

(12 citation statements)

References 93 publications

(147 reference statements)

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“…There are several studies showing that the serotonin signaling pathway can affect aldosterone synthesis in adrenocortical cells. 25…”

Section: Discussionmentioning

confidence: 99%

Subtypes of Histopathologically Classical Aldosterone-Producing Adenomas Yield Various Transcriptomic Signaling and Outcomes

Peng

Kuo³

et al. 2021

Hypertension

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There have been no reports of outcome differences between distinctive subgroups in patients with unilateral primary aldosteronism with histopathologically classical adenomas. The characteristics and incidence of complete clinical success in the patients with unilateral primary aldosteronism could be associated with the concomitant existence of multiple aldosterone-producing micronodules/nodules. Altogether, 74 classical adenomas (mean, 52.9 years and 40 men [54.1%]) were identified among 98 operated patients with unilateral primary aldosteronism. Among them accompanying multiple aldosterone-producing micronodules/nodules (group A) were identified in 38 (51.3%) of the adrenal glands; these patients showed lower likelihood (42.1%) to achieve complete clinical success than that (80.6%) of those with aldosterone-producing adenoma/nodules alone (group B, P =0.001). Additionally, group A adenomas were associated with less complete clinical success (odds ratio, 5.53, P =0.005) in the multivariable regression analysis. Group A patients also had higher baseline aldosterone production (absolute aldosterone ratio) from the contralateral adrenal gland ( P =0.039). Based on the patterns of genes with highly differential expressions as uncovered by RNA-seq analysis, Group A adenomas showed distinct transcriptomic profiles in comparison to the gene expressions from Group B adenomas. Pathway enrichment analysis revealed that HTR2B-mediated calcium pathway, in terms of HTR2B , and PLCE1 was prominently downregulated in Group A adenomas. There was 51.3% of the patients with unilateral primary aldosteronism with classical group A adenomas. These patients were more likely to have hypertension-persistence after adrenalectomy. The functional signatures of Group A adenomas showed attenuated HTR2B-mediated PLC/IP3/Ca2 + pathway; this may provide some mechanistic explanation to various clinical outcomes.

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“…There are several studies showing that the serotonin signaling pathway can affect aldosterone synthesis in adrenocortical cells. 25…”

Section: Discussionmentioning

confidence: 99%

Subtypes of Histopathologically Classical Aldosterone-Producing Adenomas Yield Various Transcriptomic Signaling and Outcomes

Peng

Kuo³

et al. 2021

Hypertension

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“…To assess the pathologic role of these mutations, it would be ideal to perform cell-based studies for each mutation. In addition to tumor somatic mutations, PA aldosterone production may be regulated by hormones that include adrenocorticotropic hormone, serotonin, or luteinizing hormone (37)(38)(39)(40)(41)(42)(43)(44).…”

Section: Introductionmentioning

confidence: 99%

Approaches to Gene Mutation Analysis Using Formalin-Fixed Paraffin-Embedded Adrenal Tumor Tissue From Patients With Primary Aldosteronism

2021

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Aldosterone production is physiologically under the control of circulating potassium and angiotensin II as well as adrenocorticotropic hormone and other secretagogues such as serotonin. The adrenal’s capacity to produce aldosterone relies heavily on the expression of a single enzyme, aldosterone synthase (CYP11B2). This enzyme carries out the final reactions in the synthesis of aldosterone and is expressed almost solely in the adrenal zona glomerulosa. From a disease standpoint, primary aldosteronism (PA) is the most common of all adrenal disorders. PA results from renin-independent adrenal expression of CYP11B2 and production of aldosterone. The major causes of PA are adrenal aldosterone-producing adenomas (APA) and adrenal idiopathic hyperaldosteronism. Our understanding of the genetic causes of APA has significantly improved through comprehensive genetic profiling with next-generation sequencing. Whole-exome sequencing has led to the discovery of mutations in six genes that cause renin-independent aldosterone production and thus PA. To facilitate broad-based prospective and retrospective studies of APA, recent technologic advancements have allowed the determination of tumor mutation status using formalin-fixed paraffin-embedded (FFPE) tissue sections. This approach has the advantages of providing ready access to archival samples and allowing CYP11B2 immunohistochemistry-guided capture of the exact tissue responsible for inappropriate aldosterone synthesis. Herein we review the methods and approaches that facilitate the use of adrenal FFPE material for DNA capture, sequencing, and mutation determination.

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“…Furthermore, paracrine regulation of aldosterone production is mediated by factors released by components of the microenvironment both in normal human adrenals and adrenals with APA, i.e. chromaffin cells, endothelial cells, adipocytes, nerve fibers and immune cells ( 28 , 33 , 41 , 42 ). Interestingly, serotonin (5-HT) released by perivascular mast cells is known to induce aldosterone production by activating the 5-hydroxytryptamine receptor 4 (5-HT4) expressed in ZG cells ( 34 ).…”

Section: Regulation Of Aldosterone Biosynthesis In the Adrenal Cortexmentioning

confidence: 99%

Vascular and hormonal interactions in the adrenal gland

Abdellatif

Fernandes-Rosa²,

Boulkroun³

et al. 2022

Front. Endocrinol.

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Primary aldosteronism is the most common form of secondary arterial hypertension, due to excessive aldosterone production from the adrenal gland. Although somatic mutations have been identified in aldosterone producing adenoma, the exact mechanisms leading to increased cell proliferation and nodule formation remain to be established. One hypothesis is that changes in vascular supply to the adrenal cortex, due to phenomena of atherosclerosis or high blood pressure, may influence the morphology of the adrenal cortex, resulting in a compensatory growth and nodule formation in response to local hypoxia. In this review, we will summarize our knowledge on the mechanisms regulating adrenal cortex development and function, describe adrenal vascularization in normal and pathological conditions and address the mechanisms allowing the cross-talk between the hormonal and vascular components to allow the extreme tissue plasticity of the adrenal cortex in response to endogenous and exogenous stimuli. We will then address recent evidence suggesting a role for alterations in the vascular compartment that could eventually be involved in nodule formation and the development of primary aldosteronism.

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Role of Mast Cells in the Control of Aldosterone Secretion

Cited by 12 publications

References 93 publications

Subtypes of Histopathologically Classical Aldosterone-Producing Adenomas Yield Various Transcriptomic Signaling and Outcomes

Subtypes of Histopathologically Classical Aldosterone-Producing Adenomas Yield Various Transcriptomic Signaling and Outcomes

Approaches to Gene Mutation Analysis Using Formalin-Fixed Paraffin-Embedded Adrenal Tumor Tissue From Patients With Primary Aldosteronism

Vascular and hormonal interactions in the adrenal gland

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