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Titolo:
Gonadotropins and cytokines affect luteal function through control of apoptosis in human luteinized granulosa cells
Autore:
Matsubara, H; Ikuta, K; Ozaki, Y; Suzuki, Y; Suzuki, N; Sato, T; Suzumori, K;
Indirizzi:
Nagoya City Univ, Sch Med, Dept Obstet & Gynecol, Mizuho Ku, Nagoya, Aichi4678601, Japan Nagoya City Univ Nagoya Aichi Japan 4678601 , Nagoya, Aichi4678601, Japan
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 4, volume: 85, anno: 2000,
pagine: 1620 - 1626
SICI:
0021-972X(200004)85:4<1620:GACALF>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; IN-VITRO FERTILIZATION; MESSENGER-RIBONUCLEIC-ACID; GROWTH-FACTOR-BETA; HUMAN CHORIONIC-GONADOTROPIN; OVARIAN FOLLICULAR-FLUID; HUMAN CORPORA-LUTEA; ADULT HUMAN OVARY; FACTOR-ALPHA; CORPUS-LUTEUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Matsubara, H Nagoya City Univ, Sch Med, Dept Obstet & Gynecol, Mizuho Ku, Kawasumi 1,Mizuho Cho, Nagoya, Aichi 4678601, Japan Nagoya City Univ Kawasumi 1,Mizuho Cho Nagoya Aichi Japan 4678601
Citazione:
H. Matsubara et al., "Gonadotropins and cytokines affect luteal function through control of apoptosis in human luteinized granulosa cells", J CLIN END, 85(4), 2000, pp. 1620-1626

Abstract

The luteal phase in the normal human menstrual cycle is known to be about 14 days. The physiological mechanisms that regulate the corpus luteum remain to be clarified, although apoptosis is reported to be involved. This study was undertaken to investigate the regulation of luteal function by gonadotropins, cytokines, and PGs, concentrating attention on the incidence of apoptosis and its molecular mechanisms in cultured human luteinized granulosacells collected at oocyte pick-up from patients undergoing in vitro fertilization and embryo transfer. Clusters of granulosa cells were pipetted in 0.1% hyaluronidase in phosphate-buffered saline. After cell separation by centrifugation using Ficoll-Paque, 1 X 10(4) viable cells/mL in RPMI 1640 medium with 10% FCS were used for experimentation. Substances added were FSH (100 ng/mL), hCG (100 ng/mL), LH (100 ng/mL), interleukin-1 beta (IL-1 beta;10 ng/mL), transforming growth factor-beta 1 (TGF beta 1; 10 ng/mL), macrophage colony- stimulating factor (M-CSF; 10 ng/mL), tumor necrosis factor-alpha (TNF alpha; 10 ng/mL), and PGF(2 alpha), (10 ng/mL). After 24-h culture at 31 C under 5% CO2 and air, cells were fixed with 4% neutral buffered formalin and stained with Hoechst 33258. Apoptotic bodies were counted undera fluorescence microscope, and immunostaining was performed using anti-Fas, Fas ligand, Bcl-2, Bar, and p53 antibodies. Incidences of apoptotic bodies in the group without substance addition were 0.7 +/- 0.2% (0 h), 5.9 +/- 0.6% (24 h), and 7.9 +/- 1.2% (48 h); spontaneous increase was significant at the latter time points. Defining the incidence at 24 h as 100%, values after treatment were: FSH, 57%; LH, 84%; hCG, 44%; IL-1 beta, 76%; TGF beta 1, 52%; M-CSF, 50%; TNF alpha, 177%; and PGF(2 alpha), 147%. Significant suppression was observed with FSH, hCG, TGF beta 1, and M-CSF (P < 0.01). On the other hand, significant induction occurred with TNF alpha and PGF(2 alpha) (P < 0.01). On immunostaining, the incidence of stained cells with anti-Fas, Fas ligand, Bar, and p53 antibody was increased after 24-h incubationwithout addition. This was reduced by hCG, TGF beta 1, and M-CSF. No stained cells were observed with anti-Bcl-2 antibody before or after incubation. In conclusion our results suggest that both gonadotropins (FSH and hCG) and cytokines (TGF beta 1 and M-CSF) may be involved in the support of lutealfunction via suppression of apoptosis, and that TNF alpha and PGF2 alpha may contribute to ovarian dysfunction and/or luteal regression via its induction in human luteinized granulosa cells. Our results also suggest that Fas, Fas ligand, p53, and Bar may play roles in this apoptosis controlled by hCG, TGF beta 1, and M-CSF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 14:52:23