ESPE Abstracts (2016) 86 P-P1-2

Mast Cells and Steroidogenesis in the Human Fetal Adrenal

Alexandre Naccachea, Estelle Louiseta, Céline Duparca, Annie Laquerrièreb, Sophie Patrierb, Sylvie Renoufa, Celso E. Gomez-Sanchezc, Kuniaki Mukaid, Hervé Lefebvrea & Mireille Castaneta

aINSERM U982, Laboratory of Differentiation & Neuronal and Neuroendocrine Communication, Institute for Research and Innovation in Biomedicine, University of Rouen, Mont-Saint-Aignan, France; bDepartment of Pathology, University Hospital of Rouen, NeoVasc Region-Inserm Team ERI28, Institute for Research and Innovation in Biomedicine, University of Rouen, Rouen, France; cEndocrine Section, Department of Medicine, G.V. (Sonny) Montgomery VA Medical Center and University of Mississippi Medical Center, Jackson, MS, USA; dDepartment of Biochemistry, School of Medicine, Keio University, Tokyo, Japan

Background: We recently demonstrated the presence of mast cells in human fetal adrenal gland from 18–20 weeks of gestation (WG) within the subcapsular layer. In the adult adrenal, mast cells have been implicated in mineralocorticoid synthesis and secretion especially in aldosterone-producing adenomas. Because similarities exist between tumors and normal fetal development and as cell-to-cell interactions involving immune cells are implicated in organogenesis, we hypothesized a role of mast cells in steroidogenesis synthesis and/or secretion in fetal adrenal development.

Objective: We thus investigated steroidogenic enzymes expression in relationship to the occurrence of mast cells in the human developing adrenal gland.

Method: Immunochemical studies were performed on 28 paraffin-embedded adrenal glands at 16–40 WG using tryptase, Scavenger Receptor class B type I (SRB1), 17α-hydroxylase (17α-OH), 3β-hydroxysteroid dehydrogenase (3βHSD), 11β-hydroxylase (11β-OH) and aldosterone synthase antibodies. Moreover, steroidogenic enzymes mRNA levels were quantified at 22, 24, 29 and 30 WG and compared to adult tissue.

Results: 3βHSD and CYP11B2 immunopositive cells were firstly detected at 18 and 24 WG respectively, within the adrenal subcapsular region close to the tryptase immunopositive cells. Conversely, no spatio-temporal correlation was observed with either 17α-OH or 11β-OH expression (detected at all fetal studied stages). In addition, SRB1 expression was early detected in the fetal zone extending to the subcapsular zone from 24 WG. QPCR confirmed the timing of steroidogenic enzyme expression reported above.

Conclusion: We show for the first time the expression profile of aldosterone and cortisol producing cells in the human fetal adrenal. Timing of the CYP11B2 expression could help better understand the pathophysiology of salt wasting syndrome in extreme premature infants. Moreover, the spatio-temporal correlation of tryptase and CYP11B2 expression suggests a contribution of mast cells in establishment of the mineralocorticoid axis. However, further studies are required to better understand this potential regulatory pathway.

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