How estrogens mediate their effect on sperm cells?\n\n

0474843 - BTÚ 2018 CZ eng A - Abstrakt
Dostálová, Pavla - Žatecká, Eva - Děd, Lukáš - Dvořáková-Hortová, Kateřina - Pěknicová, Jana
How estrogens mediate their effect on sperm cells?

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Book of abstracts XXIIIrd Symposium of Immunology and Biology of Reproduction. Vestec u Prahy: Biotechnologický ústav AVČR v. v. i., 2017 - (Kubátová, a.). s. 25-25
[XXIIIrd Symposium of Immunology and Biology of Reproduction. 18.05.2017-20.05.2017, Třešť]
Grant CEP: GA MŠMT(CZ) ED1.1.00/02.0109; GA ČR GA14-05547S
Institucionální podpora: RVO:86652036
Klíčová slova: estrogens * estrogen receptors * GPER * spermatozoa * sperm capacitation
Obor OECD: Biochemistry and molecular biology

Estrogens are steroid hormones that regulate many events during sperm cell development including spermatogenesis, epididymal maturation and sperm maturation which takes place in the female reproductive tract. The underlying mechanism of this process is not entirely clear and there is still much more to be clarified. The estrogen response is mediated through the classical estrogen receptors (ERs), namely estrogen receptor 1/alpha (ESR1), estrogen receptor 2/beta (ESR2) and a membrane G protein-coupled estrogen receptor 1 (GPER). Since the sperm nucleus is densely packed and transcriptionally inactive, the genomic estrogen signaling, where the activation of ERs leads to binding of ERs to DNA and results in changes in gene expression of target genes, cannot be involved in the estrogenic effect on sperm. On the other hand, the later described non-genomic pathway, that starts at the membrane and occurs within the seconds to minutes, is consider to be involved in estrogenic effect on sperm. We detected both classical ERs in mouse and boar sperm. The immunolocalization of ERs was in the acrosomal region of sperm head and for mouse also in the tail. More interestingly, we found two population of boar sperm based on the positivity or negativity to ESR1. Further, we showed that estrogens regulate boar sperm capacitation in a time and dose dependent manner and that only some boar individuals responded to the estrogen environment. Finally, we used agonists and antagonists of classical ERs and GPER to shed light on the involvement of estrogen receptors in mouse and boar sperm capacitation. In both model organisms, ESR1 appears to be the key receptor responsible for estrogen mediated events, while ESR2 and GPER probably play minor or no role during capacitation.
Our results indicate that estrogens activate ESR1 which leads to procapacitation effects and that the level of ESR1 expression may reflect the sensitivity of the cell to estrogen stimuli. This is of particular interest, as it is known that many endocrine disruptors change the expression of ERs and thus this may represent one of the possible mechanism how endocrine disruptors contribute to increasing fertility issues.







Trvalý link: http://hdl.handle.net/11104/0273887