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progesterone/nekrosis
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Decreased Progesterone Receptor B/A Ratio in Endometrial Cells by Tumor Necrosis Factor-Alpha and Peritoneal Fluid from Patients with Endometriosis.
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OBJECTIVE
Progesterone resistance is thought to be a major factor that contributes to progression of endometriosis. However, it is not clear what causes progesterone resistance in endometriosis. This study aimed to assess whether cytokines or peritoneal fluid can affect progesterone receptor (PR)
Effects of tumour necrosis factor alpha and interleukin-6 on progesterone and calcium ionophore-induced acrosome reaction.
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For human spermatozoa to successfully fertilize the oocyte, they need to undergo a timely acrosome reaction (AR). Factors which disturb the AR may lead to fertilization failure. The objective of this study was to investigate the effects of two cytokines namely tumour necrosis factor alpha
Hydroxyprogesterone caproate and progesterone increase tumor necrosis factor-alpha production in lipopolysaccharide stimulated whole blood from non-pregnant women.
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OBJECTIVE
Hydroxyprogesterone caproate (17-P) and progesterone have been shown to decrease the rate of preterm birth in high-risk pregnant women, but the mechanism of action is unknown. We hypothesized that 17-P or progesterone would reduce production of the pro-inflammatory cytokine, tumor necrosis
Effects of estradiol and progesterone on tumor necrosis factor alpha-induced apoptosis in human hepatoma HuH-7 cells.
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Oxidative stress, including the generation of reactive oxygen species (ROS), is known to be involved in apoptosis. Preventing apoptosis may thereby induce a malignant transformation of liver tumor cells. Estradiol (E2) is a potent endogenous antioxidant. We examined the proapoptotic role of
Modeling the effects of estradiol and progesterone on the acute phase proinflammatory axis: variability in tumor necrosis factor-α, nitric oxide, and xanthine oxidase responses to endotoxin challenge in steers.
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The severity of host response in some diseases differs between sexes, and this dimorphism has been attributed to the immunomodulating effects of reproductive steroid hormones. In females, susceptibility to disease stress has been associated with reproductive status and attributed to prevailing
Tumor necrosis factor-alpha (TNF alpha) inhibits progesterone and estradiol-17beta production from cultured granulosa cells: presence of TNFalpha receptors in bovine granulosa and theca cells.
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The aim of this study was to investigate whether functional tumor necrosis factor-alpha (TNFalpha) receptors are present in the granulosa cells and the cells of theca interna (theca cells), obtained from bovine follicles classified into one of three groups. Each group was defined as either small
Mouse endometrial tumor necrosis factor-alpha messenger ribonucleic acid and protein: localization and regulation by estradiol and progesterone.
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Tumor necrosis factor-alpha (TNF) messenger RNA (mRNA) and protein have been identified in the uteri of cycling rats, mice, and women. In this study, a mouse model was used to investigate the cell-specific expression and regulation of the TNF gene in the endometrium. Uteri from cycling and
Myometrial tumor necrosis factor alpha: cellular localization and regulation by estradiol and progesterone in the mouse.
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The expression of tumor necrosis factor alpha (TNF) protein in mouse myometrial cells on each day of the estrous cycle and after ovariectomy, with and without replacement of estradiol (E2), progesterone (P4), or E2 + P4, was investigated. TNF protein was assessed by immunocytochemistry. In addition,
Demonstration of tumor necrosis factor-alpha in preovulatory follicular fluid: its association with serum 17 beta-estradiol and progesterone.
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In the present study we have measured the concentrations of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) in preovulatory follicular fluid (FF) samples obtained from patients undergoing ovulation induction with human menopausal gonadotropin/human chorionic gonadotropin.
Concentrations of tumor necrosis factor alpha and progesterone within the bovine corpus luteum sampled by continuous-flow microdialysis during luteolysis in vivo.
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Corpora lutea (CL) of mature, nonlactating Holstein cows (n = 12) each received surgical implants of a microdialysis system between Days 12 and 16 of an estrous cycle (estrus = Day 0). Fractions from dialyzed CL were collected every 30 min for 12 h each day for 7-9 days after surgery. Concurrent
Tumor necrosis factor-alpha activates nuclear factor-kappaB but does not regulate progesterone production in cultured human granulosa luteal cells.
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BACKGROUND
The role of tumor necrosis factor-alpha (TNF-alpha) in granulosa luteal cell function and steroidogenesis is still controversial. Our aim was to examine the steroidogenic response, together with the simultaneous expression and activation of nuclear factor-kappaB (NF-kappaB), in cultured
Hormonal regulation of cytokine release by human fetal membranes at term gestation: effects of oxytocin, hydrocortisone and progesterone on tumour necrosis factor-alpha and transforming growth factor-beta 1 output.
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Inflammatory cytokines can play an important role in the biomolecular processes leading to labour by regulating prostaglandin production in intrauterine tissues. In the setting of intrauterine infection, an increased production of these cytokines by placenta, decidua and fetal membranes occurs and
Acyl chain length-specific ceramide-induced changes in intracellular Ca2+ concentration and progesterone production are not regulated by tumor necrosis factor alpha in hen granulosa cells.
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Although tumor necrosis factor alpha (TNF-alpha) has long been known to be a potent inhibitor of gonadotropin-induced cytodifferentiation in the ovaries of a variety of mammalian species, its early signal transduction events are poorly understood. We previously demonstrated that TNF-alpha induces a
Local interaction of prostaglandin F 2alpha with endothelin-1 and tumor necrosis factor-alpha on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade.
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Endothelin-1 (ET-1) and tumor necrosis factor-alpha (TNFalpha) participate in the cascade of luteolysis. Thus, in the present study the interactions of ET-1 and TNFalpha with prostaglandin F(2alpha) (PGF(2alpha)) on the release of progesterone and oxytocin (OT) within the corpus luteum (CL) were
Tumor necrosis factor (TNF)-α upregulates progesterone receptor-A by activating the NF-κB signaling pathway in human decidua after labor onset.
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To date, the relationship between inflammatory cytokines and progesterone receptors (PRs) has been little studied, although both mediate the mechanism of parturition in human deciduas. Thus, the aim of study was to investigate the role of an inflammatory cytokine, tumor necrosis factor (TNF)-α, in
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