Inhibitory effect of interferon and tumor necrosis factor on human luteal function in vitro

Wang, Han Zheng; Lu, Shu Hua; Han, Xinwei; Zhou, Wei; Sheng, Wei Xiong; Sun, Zhi Da; Gong, Yue Ting

doi:10.1016/s0015-0282(16)55439-9

Cited by 38 publications

(2 citation statements)

References 20 publications

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“…However, TNF alpha has opposing effects in luteal cells derived from mid to late luteal phase of the human, mouse and pig. In cells derived from these stages, TNF alpha inhibits the response to luteotropins in vitro (264)(265)(266)(267)(268). The TNF alpha initiated response in the pig is somewhat complex in that it can inhibit the luteotropic effect of estradiol ( 269), yet in the absence of TNF alpha, PGF2 alpha can stimulate progesterone synthesis in young corpora lutea of the pig.…”

Section: Tumor Necrosis Factor Alphamentioning

confidence: 99%

“…Interferon gamma, a type II interferon (and not a member of the TNF superfamily) can inhibit basal (266) and gonadotropin-stimulated progesterone production in human luteal cells (211,266,288); yet it has no effect on progesterone production in dispersed luteal cells derived from normally cycling cynomolgus monkeys derived from different days of the cycle (289). Treatment with interferon gamma can induce cell death in human (213), bovine (215,249,252) and mouse luteal cells (216).…”

Section: Interferon Gammamentioning

confidence: 99%

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The corpus luteum: an ovarian structure with maternal instincts and suicidal tendencies

2002

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The corpus luteum is a unique hormone-regulated, transient reproductive gland that produces progesterone, a required product for the establishment and maintenance of early pregnancy. In the absence of pregnancy the corpus luteum will cease to produce progesterone and the structure itself will regress in size over time. Although the process of luteal regression has been studied for several decades, many of the regulatory mechanisms involved in loss of function and involution of the structure are incompletely understood. More importantly, we are far from understanding how these complex mechanisms function in unison. The factor or factors responsible for initiating and mediating luteolysis are no doubt more complex than originally envisioned. Further, efforts to elucidate the mechanisms responsible for luteolysis have been complicated by different interpretations of what is 'luteolysis', discrepancies between in vitro and in vivo studies, and subsequent biases which are associated with the different methods of analyses. Moreover, the complexity of the mechanisms which regulate the life span of the corpus luteum are compounded by the presence of a heterogeneous population of cells which often respond differentially to the same ligand or stimuli. Attempts to isolate specific luteal cell types for the intention of defining intracellular signaling mechanisms have yielded valuable information. However, studies of a specific cell type taken out of context are often subject to criticism. The most obvious being that the cells are no longer maintained within their three dimensional environment. Evaluation of the corpus luteum in vivo, is not without its criticisms either. A subtle change evoked within a subpopulation of cells can be overlooked if measured in whole tissue or in mixed cell preparations. Furthermore, treatment in vivo with a single agent/ligand (i.e., prostaglandin F2 alpha) may induce a secondary ligand that is ultimately responsible for the biological response. All arguments are valid and cannot be ignored. There are secondary levels of complexity in the corpus luteum brought about by the pleiotropic actions of specific ligands. For example, one ligand can be luteotropic to a steroid producing cell and cytotoxic to a luteal endothelial cell. Furthermore, a specific cell type within the corpus luteum may respond differentially depending on the developmental stage of the luteal phase (i.e., early, mid, or late luteal phase) suggesting that the intracellular signaling pathways are key to defining ligand-induced biological responses. The purpose of this review is to culminate what is known regarding signal transduction pathways activated by initiator(s) and/or mediators of luteolysis. We recognize that an all-inclusive review describing the molecular mechanisms involved in the development, maintenance and regression of the corpus luteum would be impossible within the context of this review. There are a number of recent reviews that discuss luteal development, luteal maintenance and luteolysis with emphasis on neu...

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Section: Tumor Necrosis Factor Alphamentioning

confidence: 99%

Section: Interferon Gammamentioning

confidence: 99%

The corpus luteum: an ovarian structure with maternal instincts and suicidal tendencies

2002

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Roles of cytokines and progesterone in the regulation of the nitric oxide generating system in bovine luteal endothelial cells

Yoshioka

Acosta

Okuda

2012

Molecular Reproduction Devel

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Nitric oxide (NO) produced by luteal endothelial cells (LECs) plays important roles in regulating corpus luteum (CL) function, yet the local mechanism regulating NO generation in bovine CL remains unclear. The purpose of the present study was to elucidate if tumor necrosis factor-α (TNF), interferon γ (IFNG), and/or progesterone (P4) play roles in regulating NO generating system in LECs. Cultured bovine LECs obtained from the CL at the mid-luteal stage (Days 8-12 of the cycle) were treated for 24 hr with TNF (2.9 nM), IFNG (2.5 nM), or P4 (0.032-32 µM). NO production was increased by TNF and IFNG, but decreased by P4 (P < 0.05). TNF and IFNG stimulated the relative steady-state amounts of inducible nitric oxide synthase (iNOS) mRNA and iNOS protein expression (P < 0.05), whereas P4 inhibited relative steady-state amounts of iNOS mRNA and iNOS protein expression (P < 0.05). In contrast, endothelial nitric oxide synthase (eNOS) expression was not affected by any treatment. TNF and IFNG stimulated NOS activity (P < 0.05) and 1400W, a specific inhibitor of iNOS, reduced NO production stimulated by TNF and IFNG in LECs (P < 0.05). Onapristone, a specific P4 receptor antagonist, blocked the inhibitory effect of P4 on NO production in LECs (P < 0.05). The overall findings suggest that TNF and IFNG accelerate luteolysis by increasing NO production via stimulation of iNOS expression and NOS activity in bovine LECs. P4, on the other hand, may act in maintaining CL function by suppressing iNOS expression in bovine LECs.

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Endometriosis: Immune Cells and Their Products

Hill¹

1994

Immunobiology of Reproduction

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Inhibitory effect of interferon and tumor necrosis factor on human luteal function in vitro

Cited by 38 publications

References 20 publications

The corpus luteum: an ovarian structure with maternal instincts and suicidal tendencies

The corpus luteum: an ovarian structure with maternal instincts and suicidal tendencies

Roles of cytokines and progesterone in the regulation of the nitric oxide generating system in bovine luteal endothelial cells

Endometriosis: Immune Cells and Their Products

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