Gonadotropin-releasing hormone agonist affects rat ovarian follicle development by interfering with FSH and growth factors on the prevention of apoptosis
Apoptosis is the biological process by which follicular cells are eliminated in atretic follicles. The aim of the present study was to examine the in vitro effect of a GnRH-a (leuprolide acetate, LA) and its interactions with FSH, dibutyryl cAMP, and growth factors (IGF-I, EGF, and FGF) on follicula...
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2001
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| 024 | 7 | |2 scopus |a 2-s2.0-0034842416 | |
| 024 | 7 | |2 cas |a Bucladesine, 362-74-3; Culture Media, Serum-Free; Diethylstilbestrol, 56-53-1; Epidermal Growth Factor, 62229-50-9; Estrogens, Non-Steroidal; Fertility Agents, Female; Fibroblast Growth Factors, 62031-54-3; Follicle Stimulating Hormone, 9002-68-0; Gonadotropin-Releasing Hormone, 33515-09-2; Insulin-Like Growth Factor I, 67763-96-6; Leuprolide, 53714-56-0 | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
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| 100 | 1 | |a Parborell, F. | |
| 245 | 1 | 0 | |a Gonadotropin-releasing hormone agonist affects rat ovarian follicle development by interfering with FSH and growth factors on the prevention of apoptosis |
| 260 | |c 2001 | ||
| 270 | 1 | 0 | |m Tesone, M.; Inst. de Biol. y Med. Experimental, Obligado 2490, 1428 Buenos Aires, Argentina; email: mtesone@dna.uba.ar |
| 506 | |2 openaire |e Política editorial | ||
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| 504 | |a Tilly, J.L., Cell death and species propagation: Molecular and genetic aspects of apoptosis in the vertebrate female gonad (1998), pp. 431-452. , Lockshin RA, Zakeri Z, Tilly JL, editors. When cell die. Wiley-Liss; Tilly, J.L., Tilly, K.I., Inhibitors of oxidative stress mimic the ability of follicle-stimulating hormone to suppress apoptosis in cultured rat ovarian follicles (1995) Endocrinology, 136, pp. 242-252 | ||
| 504 | |a Tilly, J.L., Kowalski, K.I., Johnson, A.L., Hsueh, A.J., Involvement of apoptosis in ovarian follicular atresia and postovulatory regression (1991) Endocrinology, 129, pp. 2799-2801 | ||
| 504 | |a Tilly, J.L., Billig, H., Kowalski, K., Hsueh, A.J., Epidermal growth factor and basic fibroblast growth factor suppress the spontaneous onset of apoptosis in cultured rat ovarian granulosa cells and follicles by a tyrosine kinase-dependent mechanism (1992) Mol Endocrinol, 6, pp. 1942-1950 | ||
| 504 | |a Tilly, J.L., Kowalski, K.I., Schomberg, D.W., Hsuel, A.J., Apoptosis in atretic ovarian follicles is associated with selective decreases in messenger ribonucleic acid transcripts for gonadotropin receptors and cytochrome P450 aromatase (1992) Endocrinology, 131 (4), pp. 1670-1676 | ||
| 504 | |a Tilly, J.L., Tilly, K.I., Kenton, M.L., Johnson, A.L., Expression of members of the bcl-2 gene family in the immature rat ovary: Equine chorionic gonadotropin mediated inhibition of granulosa cell apoptosis is associated with decreased bax and constitutive bcl-2 and bcl-xlong messenger ribonucleic acid levels (1995) Endocrinology, 136, pp. 232-240 | ||
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| 504 | |a Zeleznick, A.J., Ihrig, L.L., Bassett, S.G., Development expression of Ca++/Mg++ -dependent endonuclease activity in rat granulosa and luteal cells (1989) Endocrinology, 125, pp. 2218-2220 | ||
| 520 | 3 | |a Apoptosis is the biological process by which follicular cells are eliminated in atretic follicles. The aim of the present study was to examine the in vitro effect of a GnRH-a (leuprolide acetate, LA) and its interactions with FSH, dibutyryl cAMP, and growth factors (IGF-I, EGF, and FGF) on follicular apoptosis in early antral ovarian follicles obtained from prepubertal DES-treated rats. Follicles cultured 24 hr in the absence of hormones showed spontaneous onset of apoptotic DNA fragmentation. The presence of FSH suppressed the spontaneous onset of apoptotic DNA fragmentation (75-85%). Quantitative estimation of DNA cleavage from ovarian follicles revealed no significant changes in DNA fragmentation after in vitro LA treatment (1-100 ng/ml). However, coincubation with LA interfered partially with the effects of FSH on apoptosis suppression. This apoptosis suppression was also obtained by treatment with dibutyryl cAMP (80%), and was partially prevented by the presence of LA in the cultures. Follicles were cultured 24 hr with FGF, EGF, or IGF-I, and these factors suppressed DNA fragmentation (70, 60, and 70% respectively), while the presence of LA (100 ng/ml) in the culture medium prevented this effect. In conclusion, we show that the rescue from apoptotic DNA fragmentation produced in early antral follicles by FSH, cAMP, and growth factors, is prevented by coincubation with LA. This GnRH analog would thus interfere in the pathway of FSH, cAMP and/or growth factors by an as yet unknown mechanism. © 2001 Wiley-Liss, Inc. |l eng | |
| 593 | |a Instituto de Biologia y Medicina Experimental (IBYME) CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina | ||
| 593 | |a Instituto de Biología y Medicina Experimental, Obligado 2490, (1428) Buenos Aires, Argentina | ||
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a EARLY ANTRAL FOLLICLES |
| 690 | 1 | 0 | |a GNRH |
| 690 | 1 | 0 | |a GROWTH FACTORS |
| 690 | 1 | 0 | |a OVARY |
| 690 | 1 | 0 | |a DIETHYLSTILBESTROL |
| 690 | 1 | 0 | |a DNA FRAGMENT |
| 690 | 1 | 0 | |a FOLLITROPIN |
| 690 | 1 | 0 | |a GONADORELIN AGONIST |
| 690 | 1 | 0 | |a GROWTH FACTOR |
| 690 | 1 | 0 | |a LEUPRORELIN |
| 690 | 1 | 0 | |a ANIMAL CELL |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a CELL CULTURE |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a DNA CLEAVAGE |
| 690 | 1 | 0 | |a FEMALE |
| 690 | 1 | 0 | |a IN VITRO STUDY |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a OVARY DEVELOPMENT |
| 690 | 1 | 0 | |a OVARY FOLLICLE |
| 690 | 1 | 0 | |a PREPUBERTY |
| 690 | 1 | 0 | |a PRIORITY JOURNAL |
| 690 | 1 | 0 | |a RAT |
| 690 | 1 | 0 | |a ANIMALS |
| 690 | 1 | 0 | |a APOPTOSIS |
| 690 | 1 | 0 | |a BUCLADESINE |
| 690 | 1 | 0 | |a CELLS, CULTURED |
| 690 | 1 | 0 | |a CULTURE MEDIA, SERUM-FREE |
| 690 | 1 | 0 | |a DIETHYLSTILBESTROL |
| 690 | 1 | 0 | |a DNA FRAGMENTATION |
| 690 | 1 | 0 | |a EPIDERMAL GROWTH FACTOR |
| 690 | 1 | 0 | |a ESTROGENS, NON-STEROIDAL |
| 690 | 1 | 0 | |a FEMALE |
| 690 | 1 | 0 | |a FERTILITY AGENTS, FEMALE |
| 690 | 1 | 0 | |a FIBROBLAST GROWTH FACTORS |
| 690 | 1 | 0 | |a FOLLICLE STIMULATING HORMONE |
| 690 | 1 | 0 | |a FOLLICULAR ATRESIA |
| 690 | 1 | 0 | |a GONADOTROPIN-RELEASING HORMONE |
| 690 | 1 | 0 | |a INSULIN-LIKE GROWTH FACTOR I |
| 690 | 1 | 0 | |a LEUPROLIDE |
| 690 | 1 | 0 | |a OVARIAN FOLLICLE |
| 690 | 1 | 0 | |a RATS |
| 690 | 1 | 0 | |a RATS, SPRAGUE-DAWLEY |
| 690 | 1 | 0 | |a SEXUAL MATURATION |
| 653 | 0 | 0 | |a lupron, Abbott, Argentina |
| 700 | 1 | |a Dain, L. | |
| 700 | 1 | |a Tesone, M. | |
| 773 | 0 | |d 2001 |g v. 60 |h pp. 241-247 |k n. 2 |p Mol. Reprod. Dev. |x 1040452X |t Molecular Reproduction and Development | |
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