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DOI 10.1111/j.1447-0756.2008.00737.x

Медицинская библиотека · The journal of obstetrics and gynaecology research · 2008

Gonadotropin-releasing hormone (GnRH)-I regulation of interleukin (IL)-1b and IL-1 receptor antagonist expression in cultured human endometrial stromal cells.

Raga Francisco, Casañ Eva M, Bonilla-Musoles Fernando

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

AIM: Human endometrium is an active site of cytokine production and action. Among these cytokines, the interleukin-1 (IL-1) system seems to be relevant to the embryonic implantation process. We have previously reported the production of GnRH-I by human blastocyst, as well as the presence of GnRH-I receptor in human endometrium. This suggests a close interaction between the immune and endocrine systems through these cytokine mediators in embryonic implantation.

METHODS

To test the relevance of this interaction during embryonic implantation, we investigated GnRH-I regulation of IL-1b and IL-1ra mRNA and protein expression in human endometrial stromal cells using quantitative competitive polymerase chain reaction and ELISA.

RESULTS

IL-1b mRNA and protein expression in cultured human endometrial stromal cells was significantly enhanced by GnRH-agonist in comparison to control groups. IL-1ra mRNA and protein was significantly decreased by GnRH-agonist in comparison to control groups. In contrast, the GnRH-antagonist ablated the regulatory effects of GnRH agonist in 1b and IL-1ra mRNA and protein levels in a dose-dependent manner.

CONCLUSIONS

In conclusion, these results suggest a possible close interaction between the immune and endocrine systems in human embryonic implantation through the classical neuropeptide hormone GnRH and its receptor.

Для цитирования: Raga Francisco, Casañ Eva M, Bonilla-Musoles Fernando. Gonadotropin-releasing hormone (GnRH)-I regulation of interleukin (IL)-1b and IL-1 receptor antagonist expression in cultured human endometrial stromal cells.. The journal of obstetrics and gynaecology research. 2008. DOI: 10.1111/j.1447-0756.2008.00737.x.

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