title: [The expression of IGF-I, TGF beta and Fas-L in granulosa cells of ovarian follicle with relation to the onset of atresia in rats].
abstract: This study was designed to investigate the effects of IGF-I, TGF beta and Fas-L on the sustaining of granulosa cells of ovarian follicle and the modulation of apoptosis of those cells, and to understand the molecular mechanisms of ovarian follicle atresia. Paraffin-embedded sections of SD rat ovary were made. Both TUNEL method and PCNA immunohistochemistry were employed to recognize atretic and healthy follicles. The expression of IGF-I, TGF beta, Fas-L and their receptors was displayed by immunostaining. The results showed that most of the granulosa cells within the healthy preantral and antral follicles were PCNA(+). At the early stage of atretic antral follicle, more than 5 granulosa cells were labelled by TUNEL method, and some granulosa cells were PCNA(+). At the late stage of atretic antral follicle, were labelled by TUNEL method. The immunoreactive products of IGF-I, IGF-IR, TGF beta, TGF beta R, Fas and Fas-L could be seen in the granulosa cells of healthy antral follicles. But, Granulosa cells were only TGF beta, TGF beta R and Fas immunopositive in all atretic antral follicles. In conclusion, combination of TUNEL method and PCNA immunochemistry is of benefit for distinguishing atretic follicles from healthy follicles. IGF-I might play an important role in stimulating proliferation of the granulosa cells and sustaining them. The lower expression or disappearance of IGF-I in the antral follicle might cause the onset of atresia. TGF beta, Fas-L and Fas might mediate apoptosis of the granulosa cells in antral follicles, causing follicle atresia. But, their effects of mediation could be inhibited as IGF-I exists in the follicles.
authors.affiliation: Department of Anatomy, School of Basic Medical Science, WCUMS, Chengdu 610041.
authors.forename: A
authors.initials: A
authors.lastname: Li
authors.forename: H
authors.initials: H
authors.lastname: Yang
authors.forename: F
authors.initials: F
authors.lastname: Wang
authors.forename: C
authors.initials: C
authors.lastname: Wei
authors.forename: J
authors.initials: J
authors.lastname: Kang
mesh_terms: D000818:Animals; D017209:Apoptosis; D053222:Fas Ligand Protein; D005260:Female; D005496:Follicular Atresia / Q000502:physiology*; D006107:Granulosa Cells / Q000378:metabolism / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008562:Membrane Glycoproteins / Q000378:metabolism*; D006080:Ovarian Follicle / Q000378:metabolism / Q000502:physiology; D010053:Ovary / Q000378:metabolism / Q000502:physiology; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000378:metabolism*
chemical_list: D053222:Fas Ligand Protein; C505662:Faslg protein, rat; D008562:Membrane Glycoproteins; D018809:Proliferating Cell Nuclear Antigen; D016212:Transforming Growth Factor beta; D007334:Insulin-Like Growth Factor I