Abstract
Ovarian glanulosa cells undergo a complex differentiation process during the growth and maturation of ovarian follicle. This process includes the acquisition of cell surface LH receptor, which mediates the granulosa cell's ability to respond to circulating LH. The results of the actions of LH on the mature granulosa cell include steroidogenesis, luteinization, and ovulation. As such, induction of the LH receptor in granulosa cells is a critical step in reproductive physiology. In the present study, we attempted to assess the effects of IGF-1 and 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) on FSH-induced LH receptor expression in rat granulosa cells to understand the actions of these factors on normal reproductive function. Treatment with FSH, as expected, produced a substantial increase in LH receptor mRNA level, and concurrent treatment with increasing concentrations of IGF-1 brought about dose-dependent increases in FSH-induced LH receptor mRNA. On the other hand, the concurrent treatment of TCDD (10 pM) resulted in a significant decrease in LH receptor after 24 h. The decay curves for LH receptor mRNA transcript showed a significant increase in the half-life after the addition of IGF-1 and a significant decrease after addition of TCDD. These data suggests a possible role for changes in LH receptor mRNA stability in the IGF-1 and TCDD induced regulation of LH receptor in rat granulosa cells. The rates of LH receptor mRNA gene transcription, assessed by nuclear run-on transcription assay, were not increased by the addition of IGF-1, but decreased by the addition of TCDD. The data of IGF-1 present that the interface between circulating hormones and paracrine/autocrine systems could provide an important mechanism to amplify the effects of gonadotropin hormones at the local level. In addition, the endocrine-disrupting effects of TCDD are, at least in part, caused by direct action on the expression of LH receptor expression in granulosa cells.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
