An ovarian phenotype of alpha 7 nicotinic receptor knockout mice

Author:

Seßenhausen Pia1ORCID,Caban Karolina M2,Kreitmair Nicole1,Peitzsch Mirko3,Stöckl Jan B2,Meinsohn Marie C4,Pépin David4,Popper Bastian5,Fröhlich Thomas2ORCID,Mayerhofer Artur1ORCID

Affiliation:

1. Biomedical Center Munich (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University of Munich, Planegg-Martinsried, Germany

2. Laboratory for Functional Genome Analysis LAFUGA, Gene Center, Ludwig Maximilian University of Munich, München, Germany

3. Institut für Klinische Chemie und Laboratoriumsmedizin, Labor Experimentelle Massenspektrometrie und Spurenelemente Universitätsklinikum Carl Gustav Carus an der Technischen Universität Dresden, Dresden, Germany

4. Pediatric Surgical Research Laboratories, Massachusetts General Hospital, and Department of Surgery, Harvard Medical School, Boston, United States

5. Biomedical Center (BMC), Core Facility Animal Models, Faculty of Medicine, Ludwig-Maximilian-University Munich, Planegg-Martinsried, Germany

Abstract

In brief Nicotinic acetylcholine receptor alpha 7 (nAChRa7), encoded by Chrna7, is expressed by various murine ovarian cells. Morphological and molecular investigations, including a proteomic study of adult Chrna7 knockout (KO) mouse ovaries, reveal the roles of these receptors in the local regulation of the ovary. Abstract Nicotinic acetylcholine receptor alpha 7 (nAChRa7), encoded by Chrna7, is involved in cellular functions ranging from synaptic transmission in neurons to regulation of inflammation, cell growth and metabolism to cell death in other cells. Our qPCR results and other studies indicated that nAChRa7 is expressed in the adult mouse ovary, while in situ hybridization and single-cell sequencing data suggested this expression may be shared by several ovarian cells, including fibroblast-like and steroidogenic stroma cells, macrophages and oocytes of small follicles. To explore a possible involvement of nAChRa7 in ovarian functions, we evaluated ovarian morphology of Chrna7-null mutant adult mice (KO) and wildtype mice (WT; 3 months, metestrus) by performing immunohistochemistry, qPCR studies, measurements of serum progesterone and proteomic analyses. The evaluation of serial sections indicated fewer primordial follicles but similar numbers of primary, secondary and tertiary follicles, as well as corpora lutea in KO and WT mice. Atresia was unchanged. Serum progesterone and mRNA levels of proliferation and most apoptosis markers were not changed, yet two typical macrophage markers were elevated. Furthermore, the proteomes of KO ovaries were significantly altered with 96 proteins increased and 32 decreased in abundance in KOs compared to WTs. Among the elevated proteins were markers for stroma cells. Hence, the lack of nAChRa7 causes changes in small follicle counts and alterations of the ovarian stroma cells. The ovarian phenotype of Chrna7 mutant mice links this channel protein to the local regulation of ovarian cells, including stroma cells.

Publisher

Bioscientifica

Subject

Cell Biology,Obstetrics and Gynecology,Endocrinology,Embryology,Reproductive Medicine

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