PUBLICATION
Oestrogen-induced androgen insufficiency results in a reduction of proliferation and differentiation of spermatogonia in the zebrafish testis
- Authors
- de Waal, P., Leal, M., García-López, A., Liarte, S., de Jonge, H., Hinfray, N., Brion, F., Schulz, R., and Bogerd, J.
- ID
- ZDB-PUB-090511-12
- Date
- 2009
- Source
- The Journal of endocrinology 202(2): 287-297 (Journal)
- Registered Authors
- Bogerd, Jan
- Keywords
- none
- MeSH Terms
-
- Androgens/deficiency*
- Animals
- Cell Differentiation/drug effects*
- Cell Proliferation/drug effects*
- Down-Regulation
- Estradiol/pharmacology*
- Estrogens/pharmacology*
- Feedback, Physiological
- Gonadotropins/antagonists & inhibitors
- Male
- Spermatids/cytology
- Spermatogonia/cytology*
- Steroids/biosynthesis
- Testis/cytology*
- Testis/drug effects
- Testis/metabolism
- Testis/physiology
- Testosterone/analogs & derivatives
- Testosterone/biosynthesis
- Zebrafish
- PubMed
- 19420009 Full text @ J. Endocrinol.
Citation
de Waal, P., Leal, M., García-López, A., Liarte, S., de Jonge, H., Hinfray, N., Brion, F., Schulz, R., and Bogerd, J. (2009) Oestrogen-induced androgen insufficiency results in a reduction of proliferation and differentiation of spermatogonia in the zebrafish testis. The Journal of endocrinology. 202(2):287-297.
Abstract
Androgens can induce complete spermatogenesis in immature or prepubertal teleost fish. However, many aspects of the role of androgens in adult teleost spermatogenesis have remained elusive. Since oestrogens inhibit androgen synthesis, we used an oestrogen-induced androgen depletion model to identify androgen-dependent stages during adult zebrafish spermatogenesis. Exposure to 10 nM 17beta-oestradiol in vivo at least halved the mass of differentiating germ cells (from type B spermatogonia to spermatids), while type A spermatogonia accumulated. Studies on the cellular dynamics revealed that a reduction of spermatogonial proliferation together with an inhibition of their differentiation to type B spermatogonia were the basis for the oestrogen-mediated disturbance of spermatogenesis. The capacity of the zebrafish testis to produce 11-ketotestosterone as well as the expression of steroidogenesis-related genes was markedly decreased after in vivo oestrogen exposure. Moreover, the androgen release response to recombinant zebrafish luteinizing hormone was lost after oestrogen exposure. We conclude that oestrogen exposure caused a state of androgen insufficiency in adult male zebrafish. Since the down-regulation of the steroidogenic system as well as disturbance of spermatogenesis in testicular explants exposed to 17beta-oestradiol ex vivo was much less severe than after in vivo exposure, the main inhibitory effect appears to be exerted via feedback inhibition of gonadotropin release. This experimental set-up helped to identify spermatogonial proliferation and their differentiation as androgen targets in adult zebrafish spermatogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping