The number and quality of ovarian follicles are important in determining the longevity and integrity of female fertility. It is well known that the survival and development of these follicles including ovulation, which results in the release of viable oocytes ready for fertilization, are controlled primarily by the gonadotropins. However, there is increasing evidence which suggests that there are several other factors such as the bone morphogenetic proteins (BMPs) which co-regulate ovarian function along with gonadotropins.
In our recent studies in an attempt to shed light on the mechanism of action of BMPs, we have created an in vivo mouse model with attenuated BMP signalling using passive immunization against BMPR1B and BMP4. The aim of this study was to investigate the localization of BMP receptor 1B (BMPR1B), FSHR and LHR in the ovaries of mice treated with anti-BMPR1B, and anti-BMP4 with and without exogenous gonadotropins (eCG).
BMPR1B was expressed in all follicle stages, FSHR was detected in primary follicles onward and LHR was absent in primary follicles but appeared in later stages. Quantitative analysis based on the intensity of fluorescent signals showed that the expression of BMPR1B, FSHR and LHR significantly increased in the granulosa cells of the pre-ovulatory and secondary follicles in mice treated with anti-BMPR1B.
Mice treated with anti-BMP4 show that the expression of BMPR1B and FSHR but not LHR increased significantly in pre-ovulatory follicles only with no effects observed in any other stages. The pre-ovulatory follicles in mice treated with eCG showed increased BMPR1B and FSHR but not LHR expression.
These results together with our previous reports in sheep and mice confirm that the attenuation of BMP signalling system can be an effective approach to sustain the development of growing follicles, ovulation and consequently overall female fertility.