Role of Tumor Necrosis Factor in Preovulatory Follicles of Swine

Prange‐Kiel, Janine; Kreutzkamm, Claudia; Wehrenberg, Uwe; Rune, Gabriele M.

doi:10.1095/biolreprod65.3.928

Cited by 38 publications

(29 citation statements)

References 33 publications

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“…Primary cultured bovine granulosa cells underwent apoptosis after treatment with TNF-α and IFN-γ, but not by treatment with TNF-α alone [65]. Addition of recombinant TNF-α to primary cultured porcine granulosa cells significantly increased Ki-67-positive cells (proliferating cells) as well as terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells (apoptotic cells), indicating that TNF-α could induce both cell proliferation and cell death in granulosa cells [81]. TNF-α likely induces follicular atresia, since its mRNA expression is higher in bovine granulosa cells of subordinate follicles than in those of dominant follicles [78].…”

Section: Tumor Necrosis Factor-alpha (Tnf-α)mentioning

confidence: 99%

Follicular Growth and Atresia in Mammalian Ovaries: Regulation by Survival and Death of Granulosa Cells

et al. 2012

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Abstract. The mammalian ovary is an extremely dynamic organ in which a large majority of follicles are effectively eliminated throughout their reproductive life. Due to the numerous efforts of researchers, mechanisms regulating follicular growth and atresia in mammalian ovaries have been clarified, not only their systemic regulation by hormones (gonadotropins) but also their intraovarian regulation by gonadal steroids, growth factors, cytokines and intracellular proteins. Granulosa cells in particular have been demonstrated to play a major role in deciding the fate of follicles, serving molecules that are essential for follicular growth and maintenance as well as killing themselves by an apoptotic process that results in follicular atresia. In this review, we discuss the factors that govern follicular growth and atresia, with a special focus on their regulation by granulosa cells. First, ovarian folliculogenesis in adult life is outlined. Then, we explain about the regulation of follicular growth and atresia by granulosa cells, in which hormones, growth factors and cytokines, death ligand-receptor system and B cell lymphoma/leukemia 2 (BCL2) family members (mitochondriamediated apoptosis) are further discussed. O varian follicle development is a process regulated by various endocrine, paracrine and autocrine factors that act coordinately to select follicles for ovulation. The vast majority of follicles (more than 99% of all follicles) fail to reach the preovulatory stage, but instead undergo the degenerative process called atresia. After the endocrine mechanisms by a hypothalamo-pituitary-ovarian axis were elucidated, granulosa cells have been the focus of interest in numerous studies that examined the mechanisms of follicular growth and atresia. From in vivo and in vitro experiments, factors secreted from granulosa cells, including gonadal steroids, growth factors, and cytokines, were shown to be essential for the survival of granulosa cells and their eventual follicular growth. Moreover, granulosa cells were observed as initial cell populations that underwent apoptosis in atretic follicles earlier than oocytes and theca cells, suggesting their role as the initiator of follicular atresia. Factors so far associated with apoptosis expressed in granulosa cells were shown to be crucial for the precise regulation of follicular growth and atresia. Here, we provide an overview of ovarian folliculogenesis in adult life and then discuss the intraovarian factors that govern follicular growth and atresia, with special emphasis on the precise mechanisms of granulosa cell survival and death.

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Section: Tumor Necrosis Factor-alpha (Tnf-α)mentioning

confidence: 99%

Follicular Growth and Atresia in Mammalian Ovaries: Regulation by Survival and Death of Granulosa Cells

et al. 2012

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“…PrangeKiel et al [24] showed that TNF induced both cell proliferation and apoptosis in primary cultured porcine granulosa cells. In healthy follicles, Nakayama et al [25] detected intense staining for TNFα and TRAF2 and their mRNAs in the outer zone of the granulosa layer, where many proliferating cells but no apoptotic cells were observed.…”

Section: Tnfα and Tnfrs In Granulosa Cell Apoptosismentioning

confidence: 99%

Role of Cell-Death Ligand-Receptor System of Granulosa Cells in Selective Follicular Atresia in Porcine Ovary

et al. 2011

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Abstract. In the mammalian ovary, more than 99% of follicles degenerate without ovulation and few oocytes ovulate and succeed to the next generation. Granulosa cell apoptosis plays a critical role in this process, follicular atresia. However, the molecular mechanisms responsible for the regulation of granulosa cell apoptosis have not been clarified. Death ligand and receptor systems are major apoptosis-inducing factors. This review describes the granulosa cell apoptosis via death ligand and receptor systems during follicular atresia in the porcine ovary.

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“…In primary cultured granulosa cells prepared from large antral follicles of porcine ovaries, TNFα could induce both cell proliferation and cell death [122]. However, there has been no in vivo confirmed evidence of whether TNFα acts as an apoptotic factor or as a survival/anti-apoptotic factor in porcine ovarian follicles.…”

Section: Tnfα and Tnf-receptor Systemmentioning

confidence: 99%

Regulation Mechanism of Selective Atresia in Porcine Follicles: Regulation of Granulosa Cell Apoptosis during Atresia

Manabe

Goto

Matsuda‐Minehata

et al. 2004

Journal of Reproduction and Development

194

139

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Abstract. More than 99% of follicles undergo a degenerative process known as "atresia", in mammalian ovaries, and only a few follicles ovulate during ovarian follicular development. We have investigated the molecular mechanism of selective follicular atresia in mammalian ovaries, and have reported that follicular selection dominantly depends on granulosa cell apoptosis. However, we have little knowledge of the molecular mechanisms that control apoptotic cell death in granulosa cells during follicle selection. To date, at least five cell death ligand-receptor systems [tumor necrosis factor (TNF)α and receptors, Fas (also called APO-1/CD95) ligand and receptors, TNF-related apoptosisinducing ligand (TRAIL; also called APO-2) and receptors, APO-3 ligand and receptors, and PFG-5 ligand and receptors] have been reported in granulosa cells of porcine ovaries. Some cell death ligand-receptor systems have "decoy" receptors, which act as inhibitors of cell death ligand-induced apoptosis in granulosa cells. Moreover, we showed that the porcine granulosa cell is a type II apoptotic cell, which has the mitochondrion-dependent apoptosis-signaling pathway. Briefly, the cell death receptor-mediated apoptosis signaling pathway in granulosa cells has been suggested to be as follows. (1) (7) Cytochrome c and ATP-dependent oligimerization of apoptotic protease-activating factor-1 (Apaf-1) allows recruitment of procaspase-9 into the apoptosome complex. Activation of procaspase-9 is mediated by means of a conformational change. (8) The activated caspase-9 cleaves downstream effector caspases (caspase-3). (9) Finally, apoptosis is induced. Recently, we found two intracellular inhibitor proteins [cellular FLICE-like inhibitory protein short form (cFLIPS) and long form (cFLIPL)], which were strongly expressed in granulosa cells, and they may act as anti-apoptotic/survival factors. Further in vivo and in vitro studies will elucidate the largely unknown molecular mechanisms, e. g.

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Role of Tumor Necrosis Factor in Preovulatory Follicles of Swine

Cited by 38 publications

References 33 publications

Follicular Growth and Atresia in Mammalian Ovaries: Regulation by Survival and Death of Granulosa Cells

Follicular Growth and Atresia in Mammalian Ovaries: Regulation by Survival and Death of Granulosa Cells

Role of Cell-Death Ligand-Receptor System of Granulosa Cells in Selective Follicular Atresia in Porcine Ovary

Regulation Mechanism of Selective Atresia in Porcine Follicles: Regulation of Granulosa Cell Apoptosis during Atresia

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