Fas Antigen-Mediated Apoptosis in Human Granulosa/luteal Cells1

Quirk, Susan M.; Cowan, Robert G.; Joshi, Shree; Henrikson, Katherine P.

doi:10.1095/biolreprod52.2.279

Cited by 178 publications

(149 citation statements)

References 45 publications

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“…Many previous reports, including ours, demonstrated expression of Fas on granulosa cells. [31][32][33][34][35][36][37][38] A few reports suggested expression of Fas on oocytes 32,38,39 although we could not detect it. On the other hand, Kit expression was shown to be restricted on oocytes but not on granulosa cells in follicles, 13,18,55 while deficiency of Kit leads to Fas-induced loss of granulosa cells as well as oocytes.…”

Section: Discussionmentioning

confidence: 78%

“…28 In female gonads, we and others demonstrated that Fas is expressed on granulosa cells of various follicles and luteal cells. [31][32][33][34][35][36][37][38] A few reports showed Fas expression on oocytes, but we have not been able to confirm this. 32,38,39 The expression on granulosa and luteal cells suggests that Fas is involved in follicular atresia and luteolysis for the gonadal homeostasis of adult mice.…”

Section: Introductionmentioning

confidence: 86%

“…10 We investigated whether Fas is involved in these events because we and other groups previously showed the expression of Fas in both male and female gonads. [31][32][33][34][35][36][37][38]41,[43][44][45][46] To clarify whether Fas is involved in germ cell degeneration in the gonads of W mutant mice, we generated double-mutant mice (W v /W v :Fas À/À ) by intercrossing the spontaneous Kit mutant W v mice with Fas-deficient mice against the same C57BL/6 background.…”

Section: Analysis Of Double-mutant Micementioning

confidence: 99%

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Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

et al. 2003

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Kit and its ligand stem cell factor (SCF) play a fundamental role in hematopoiesis, melanogenesis and gametogenesis. Homozygous W v mutant mice with a mutation in kit show abnormalities in these cell lineages. Fas is a member of the death receptor family inducing apoptosis. In this study, we generated double-mutant mice (W v /W v :Fas À/À ) and analyzed histologically their reproductive organs. In testes and ovaries of the double-mutant mice, testicular germ cells and oocytes were detected, respectively, whereas the same-aged W v /W v mice contained neither cells. In addition, inhibition of Kit signals by administration of anti-Kit mAb, which induces degeneration of testicular germ cells in vivo in wild-type mice, did not cause degeneration in Fas-deficient mice. In testicular germ cells of W v /W v mutant mice, an increase of Fas expression was observed in spermatogonia. Further, in vitro treatment with SCF was shown to downregulate Fas on fibroblasts expressing exogenous Kit through activation of PI3-kinase/Akt. All the results clearly indicate that Fasmediated apoptosis is involved in germ cell degeneration accompanied by defects in Kit-mediated signals, and Kit signaling negatively regulates Fas-mediated apoptosis in vivo.

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 86%

Section: Analysis Of Double-mutant Micementioning

confidence: 99%

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Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

et al. 2003

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“…This result suggests that the amount of bax present in granulosa cells that maintain a constitutive level of bcl-2 expression may be linked to the induction of granulosa cell apoptosis and follicular atresia mediated by heat-stress. It is known that another apoptotic signaling cascade, the Fas/Fas ligand (FasL) system, can lead to granulosa cell apoptosis (Quirk et al 1995, Hakuno et al 1996, Kim et al 1998). Thus, it is possible that heat stress stimulates the Fas/FasL cascade in the granulosa cells of growing follicles.…”

Section: Discussionmentioning

confidence: 99%

Heat stress diminishes gonadotropin receptor expression and enhances susceptibility to apoptosis of rat granulosa cells

Shimizu¹,

Ohshima²,

Ozawa³

et al. 2005

Reproduction

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Heat stress inhibits ovarian follicular development in mammalian species. We hypothesized that heat stress inhibits the function of follicular granulosa cells and suppresses follicular development. To test this, immature female rats were injected with pregnant mare serum gonadotropin (PMSG) at 48 h after the start of temperature treatment (control: 25 8C, 50% RH; heat stress: 35 8C, 70% Relative Humidity). The ovaries and granulosa cells of follicles at different developmental stages were analyzed for gonadotropin receptor levels and aromatase activity; estradiol levels were measured in follicular fluid. Before injection, heat stress diminished only the amount of FSH receptor on granulosa cells of antral follicles. During PMSG-stimulated follicular development, heat stress strongly inhibited gonadotropin receptor levels and aromatase activity in granulosa cells, and estradiol levels in the follicular fluid of early antral, antral and preovulatory follicles. To examine apoptosis and mRNA levels of bcl-2 and bax in granulosa cells, follicles harvested 48 h after PMSG injection were cultured in serum-free conditions. Heat-stressed granulosa cells showed a time-dependent increase in apoptosis. The bcl-2 mRNA levels were similar in control and heat-stressed granulosa cells; bax mRNA levels were increased in heat-stressed granulosa cells. According to these results, heat stress inhibits expression of gonadotropin receptors in granulosa cells and attenuates estrogenic activity of growing follicles, granulosa cells of heat-stressed follicles are susceptible to apoptosis, and the bcl2/bax system is not associated with heat-stress-induced apoptosis of granulosa cells. Our study suggests that decreased numbers and function of granulosa cells may cause ovarian dysfunction in domestic animals in summer.

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“…Cell death ligand and receptor systems [such as the Fas ligand (FasL)/Fas system and TNF relating apoptosis inducing ligand (TRAIL)/TRAIL-receptor system] mediate apoptosis during follicular aresia in porcine ovaries [18][19][20][21][22][23][24][25][26][27]. In porcine granulosa cells, apoptosis is regulated by a cell death ligand and receptor system, TRAIL/TRAIL-R, as follows [22].…”

mentioning

confidence: 99%

Molecular Characteristics of Porcine Fas-associated Death Domain (FADD) and Procaspase-8

Inoue

Matsuda‐Minehata

Goto

et al. 2007

Journal of Reproduction and Development

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Abstract. To reveal the intracellular signal transduction molecules involved in granulosa cell apoptosis in porcine ovarian follicles, we cloned the porcine Fas-associated death domain (FADD), an adaptor protein for the cell death receptor, and procaspase-8, an initiator caspase. Porcine FADD (pFADD) was 636 bp (211 amino acids: aa) long and showed 74.0 and 65.4% homology with human and murine FADD, respectively. Porcine procaspase-8 (pprocaspase-8) was 1,431 bp (476 aa) long and 70.6 and 63.4% homologous with human and murine procaspase-8, respectively. To confirm the apoptosis-inducing abilities, we constructed pFADD and pprocaspase-8 cDNA expression vectors with enhanced green fluorescence protein (EGFP) and then transfected them into human uterine cervix tumor (HeLa-K), human granulosa cell-derived (KGN), murine granulosa-derived tumor (KK1), and porcine granulosa cell-derived (JC410) cells. When pFADD and pprocaspase-8 were overexpressed, cell death was induced in these transfected cells. However when caspase-inhibitor p35 was cotransfected, cell death was inhibited. The pFADD and pprocaspase-8 genes are well conserved, as are the physiological functions of their products. Key words: Apoptosis, Caspase-8, Fas-associated death domain (FADD), Granulosa cell, Porcine ovary (J. Reprod. Dev. 53: [427][428][429][430][431][432][433][434][435][436] 2007) poptosis is an important phenomenon involved i n c e l l s u r v i v a l a n d / o r d e a t h d u r i n g differentiation and development [1,2]. The death ligand and receptor systems are considered to be apoptosis-inducing factors [3][4][5][6][7]. Death receptors, which belong to the tumor necrosis factor (TNF) receptor family, are membrane-binding proteins with a death domain (DD) in their intracellular regions. An adaptor protein, such as Fasassociating death domain protein (FADD), which has a DD in the C-terminal region and a death effector domain (DED) in the N-terminal region, is recruited when each specific ligand binds to its r e c e p t o r [ 8 -1 0 ] . T h e n , F A D D b i n d s w i t h procaspase-8 (also called FLICE), which has two DEDs in the N-teminal region [11,12]. These molecules compose the death-inducing signaling complex (DISC). As a result of the proteolytic autoactivation of procaspase-8 [13], subunit protein 18 (p18) and 11 (p11) are released into the cytoplasm and reform a proteolytic component that c l e a v e s m a n y s u b s t r a t e p r o t e i n s , s u c h a s

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Fas Antigen-Mediated Apoptosis in Human Granulosa/luteal Cells1

Cited by 178 publications

References 45 publications

Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

Involvement of death receptor Fas in germ cell degeneration in gonads of Kit-deficient Wv/Wv mutant mice

Heat stress diminishes gonadotropin receptor expression and enhances susceptibility to apoptosis of rat granulosa cells

Molecular Characteristics of Porcine Fas-associated Death Domain (FADD) and Procaspase-8

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