PMID- 14580651 OWN - NLM STAT- MEDLINE DCOM- 20040316 LR - 20190823 IS - 0093-691X (Print) IS - 0093-691X (Linking) VI - 60 IP - 9 DP - 2003 Dec TI - The effect of follicle-stimulating hormone on follicular development, granulosa cell apoptosis and steroidogenesis and its mediation by insulin-like growth factor-I in the goat ovary. PG - 1691-704 AB - The effect of FSH on goat follicular development, granulosa cell apoptosis and steroidogenesis and its mediation by insulin-like growth factor (IGF)-I were studied through both in vivo and in vitro experiments. The FSH treatment was begun on Day 9 after estrus and consisted of injections twice a day for 3 days in decreasing doses (7.5-7.5-5.0-5.0-2.5-2.5 mg). Does in both treatment and control groups were slaughtered for ovaries on Day 12. Granulosa cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Expression of IGF-I and IGF-II mRNA was determined by RT-PCR, while concentrations of progesterone (P4), estradiol (E2), IGF-I and IGF-II were measured by radioimmunoassay (RIA). Following parameters increased significantly (P<0.05) after the FSH treatment: follicle number (5.0+/-1.5 versus 9.0+/-2.0 per ovary), the level of E2 (0.1+/-0.1 ng/ml versus 0.7+/-0.2 ng/ml), the E2/P4 ratio (0.7+/-0.4 versus 4.7+/-3.0) and the concentrations of IGF-I (0.5+/-0.2 ng/ml versus 119.4+/-15.1 ng/ml) and IGF-II (0.12+/-0.03 ng/ml versus 40.9+/-18.7 ng/ml) in follicular fluid of the medium sized (3-5 mm) follicles and in the ovarian cortex the relative quantity of IGF-I mRNA (0.37+/-0.17 versus 0.90+/-0.12 Max OD). In contrast, the ratio of apoptotic granulosa cells in these follicles was reduced significantly (0.53+/-0.1 versus 0.10+/-0.01, P<0.05). In large (>5 mm) follicles, however, only the follicle number (2.3+/-0.7 versus 7.0+/-1.5 per ovary) and the level of IGF-I (38.4+/-11.0 ng/ml versus 87.3+/-13.9 ng/ml) increased significantly (P<0.05), whereas other values did not change. In vitro culture of granulosa cells showed that FSH significantly (P<0.05) enhanced IGF-I production (12.7+/-2.1 ng/ml versus 26.+/-21.9 ng/ml) by these cells, and both FSH and IGF-I reduced the ratios of apoptotic cells (from 0.7+/-0.07 to 0.3+/-0.1 and 0.2+/-0.04, respectively) and the effect was additive when both were used together. H89, the PKA pathway inhibitor, blocked the effect of FSH on granulosa cell apoptosis and IGF-I production in vitro. These results indicated that FSH mainly enhanced the development of medium sized follicles in the goat by suppressing the apoptosis of granulosa cells via increasing production of IGF-I and steroids, possibly through the PKA pathway. FAU - Yu, Yuansong AU - Yu Y AD - College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, PR China. FAU - Li, Wei AU - Li W FAU - Han, Zhengbin AU - Han Z FAU - Luo, Mingjiu AU - Luo M FAU - Chang, Zhongle AU - Chang Z FAU - Tan, Jinghe AU - Tan J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Theriogenology JT - Theriogenology JID - 0421510 RN - 0 (Steroids) RN - 67763-96-6 (Insulin-Like Growth Factor I) RN - 67763-97-7 (Insulin-Like Growth Factor II) RN - 9002-68-0 (Follicle Stimulating Hormone) SB - IM MH - Animals MH - Apoptosis/*drug effects/physiology MH - Dose-Response Relationship, Drug MH - Female MH - Follicle Stimulating Hormone/*pharmacology MH - Goats/metabolism/*physiology MH - Granulosa Cells/drug effects/pathology MH - In Situ Nick-End Labeling/veterinary MH - Insulin-Like Growth Factor I/metabolism MH - Insulin-Like Growth Factor II/metabolism MH - Ovarian Follicle/drug effects/*physiology MH - Ovary/physiology MH - Radioimmunoassay/veterinary MH - Random Allocation MH - Reverse Transcriptase Polymerase Chain Reaction/veterinary MH - Steroids/*biosynthesis EDAT- 2003/10/29 05:00 MHDA- 2004/03/18 05:00 CRDT- 2003/10/29 05:00 PHST- 2003/10/29 05:00 [pubmed] PHST- 2004/03/18 05:00 [medline] PHST- 2003/10/29 05:00 [entrez] AID - S0093691X03002887 [pii] AID - 10.1016/j.theriogenology.2003.08.001 [doi] PST - ppublish SO - Theriogenology. 2003 Dec;60(9):1691-704. doi: 10.1016/j.theriogenology.2003.08.001.