Receptors for insulin-like growth factor-I and tumor necrosis factor-alpha are hormonally regulated in bovine granulosa and thecal cells.
Mastitis induces release of tumor necrosis factor-alpha (TNFalpha) and has been linked with reduced reproductive performance. To further elucidate the role and mechanism of action of TNFalpha on ovarian cells, the effect of TNFalpha on insulin-like growth factor-I (IGF-I)-induced steroidogenesis and IGF-I binding sites in granulosa and thecal cells as well as the hormonal regulation of TNFalpha receptors were evaluated. Granulosa and thecal cells were obtained from small (1-5mm) and large (> or =8mm) bovine ovarian follicles, respectively, and cultured for 3-4 days. During the last 2 days of culture, cells were treated with various hormones and steroid production and specific binding of 125I-IGF-I and 125I-TNFalpha was determined. Two-day treatment with 30 ng/ml of TNFalpha decreased (P<0.05) IGF-I-induced estradiol production by granulosa cells and IGF-I-induced androstenedione production by thecal cells. Two-day treatment with 10 and 30ng/ml of TNFalpha decreased (P<0.05) specific binding of 125I-IGF-I to thecal cells, but had no effect on specific binding of 125I-IGF-I to granulosa cells, or on specific binding of 125I-IGF-II to thecal cells. TNFalpha did not compete for 125I-IGF-I binding to granulosa or thecal cells whereas unlabeled IGF-I suppressed 125I-IGF-I binding. Insulin inhibited (P<0.10) whereas FSH had no effect on the number of specific 125I-TNFalpha binding sites in granulosa cells. In contrast, LH increased (P<0.10) whereas insulin had no effect on specific 125I-TNFalpha binding sites in thecal cells. These results suggest that IGF-I and TNFalpha receptors in granulosa and thecal cells are regulated by hormones differentially.
Spicer
L J
LJ
Department of Animal Science, Oklahoma State University, Stillwater, OK 74078, USA. igf1leo@kstate.edu
D000735:Androstenedione / Q000096:biosynthesis; D000818:Animals; D002417:Cattle / Q000378:metabolism*; D002478:Cells, Cultured; D004958:Estradiol / Q000096:biosynthesis; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D006107:Granulosa Cells / Q000378:metabolism*; D006728:Hormones / Q000494:pharmacology*; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism / Q000494:pharmacology; D007335:Insulin-Like Growth Factor II / Q000378:metabolism; D007986:Luteinizing Hormone / Q000494:pharmacology; D006080:Ovarian Follicle / Q000166:cytology; D017526:Receptor, IGF Type 1 / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D011994:Recombinant Proteins / Q000378:metabolism / Q000494:pharmacology; D013799:Theca Cells / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000494:pharmacology
D006728:Hormones; D007328:Insulin; D018124:Receptors, Tumor Necrosis Factor; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D000735:Androstenedione; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D017526:Receptor, IGF Type 1