PUBLICATION
PGE2 inhibits spermatogonia differentiation in zebrafish: interaction with Fsh and an androgen
- Authors
- Crespo, D., Lemos, M.S., Zhang, Y.T., Safian, D., Norberg, B., Bogerd, J., Schulz, R.
- ID
- ZDB-PUB-191011-30
- Date
- 2019
- Source
- The Journal of endocrinology 244(1): 163-175 (Journal)
- Registered Authors
- Bogerd, Jan, Schulz, Rüdiger W.
- Keywords
- none
- MeSH Terms
-
- Androgens/metabolism*
- Animals
- Cell Culture Techniques
- Cell Differentiation/genetics*
- Dinoprostone/physiology*
- Follicle Stimulating Hormone/metabolism*
- Male
- Receptors, Prostaglandin E, EP4 Subtype/metabolism
- Signal Transduction/genetics
- Spermatogonia/metabolism*
- Testis/cytology
- Zebrafish
- PubMed
- 31600720 Full text @ J. Endocrinol.
Citation
Crespo, D., Lemos, M.S., Zhang, Y.T., Safian, D., Norberg, B., Bogerd, J., Schulz, R. (2019) PGE2 inhibits spermatogonia differentiation in zebrafish: interaction with Fsh and an androgen. The Journal of endocrinology. 244(1):163-175.
Abstract
Changes in zebrafish testicular gene expression induced by follicle-stimulating hormone (Fsh) or anti-Mullerian hormone (Amh) suggested that Amh inhibition and Fsh stimulation of spermatogenesis involved up- and down-regulation, respectively, of prostaglandin (PG) signaling. We found that Sertoli cells contacting type A undifferentiated (Aund) and differentiating (Adiff) spermatogonia expressed a key-enzyme of PG production (Ptgs2); previous work showed that Sertoli cells contacting Adiff and B spermatogonia and spermatocytes showed ptges3b expression, an enzyme catalyzing PGE2 production. In primary testis tissue cultures, PGE2, but not PGD2 or PGF2α, reduced the mitotic activity of Adiff and their development into B spermatogonia. Vice versa, inhibiting PG production increased the mitotic activity of Adiff and B spermatogonia. Studies with pharmacological PG receptor antagonists suggest that an Ep4 receptor mediates the inhibitory effects on the development of spermatogonia, and cell sorting experiments indicated this receptor is expressed mainly by testicular somatic cells. Combined inhibition of PG and steroid production moreover reduced the mitotic activity of Aund spermatogonia and led to their partial depletion, suggesting that androgens (and/or other testicular steroids), supported by PGE2, otherwise prevent depletion of Aund. Androgens also decreased testicular PGE2 production, increased the transcript levels of the enzyme catabolizing PGs and decreased PGE2 receptor ptger4b transcript levels. Also Fsh potentially reduced, independent of androgens, PGE2 production by decreasing ptges3b transcript levels. Taken together, our results indicate that PGE2, via Ep4 receptors, favors self-renewal in conjunction with androgens and, independent of Fsh and androgens, inhibits differentiating divisions of spermatogonia.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping