Tumor necrosis factor (TNF)-α upregulates progesterone receptor-A by activating the NF-κB signaling pathway in human decidua after labor onset

Jiang, Ziyan; Guo, Yan; Ren, Huaibin; Zou, Yanfen; Fan, Meiqiang; Lv, Yan; Han, Ping; De, Wei; Sun, Lei

doi:10.1016/j.placenta.2011.09.004

Cited by 16 publications

(12 citation statements)

References 39 publications

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“…44 In a recent study, decidual cell TNF immunostaining, and protein levels, the PR-A/PR-B ratio and type II cyclooxygenase were increased significantly in association with the onset of labor. 45 Interestingly, in quiescent (ie, not in labor) decidual cells, TNF induced a concentration-dependent increase in NF-kB activity was associated with increased levels of PR-A and type II cyclooxygenase, which suggests a role for TNF in regulating functional progesterone withdrawal. 45 Similarly, abruptionassociated preterm delivery is associated with thrombin-mediated functional progesterone withdrawal the involves PR-A and PR-B in decidual cells.…”

Section: Commentmentioning

confidence: 96%

“…45 Interestingly, in quiescent (ie, not in labor) decidual cells, TNF induced a concentration-dependent increase in NF-kB activity was associated with increased levels of PR-A and type II cyclooxygenase, which suggests a role for TNF in regulating functional progesterone withdrawal. 45 Similarly, abruptionassociated preterm delivery is associated with thrombin-mediated functional progesterone withdrawal the involves PR-A and PR-B in decidual cells. 46 There is no information on how mPRs change at the end of gestation.…”

Section: Commentmentioning

confidence: 96%

“…Clinical trials suggest that progestogen prophylaxis reduces the risk of preterm birth in at-risk women. 22,[44][45][46][47][48][49][50] However, observations regarding the capacity for progestogen therapy to prevent PPROM specifically are lacking. 22,[47][48][49][50] In most studies, either PPROM rates were not reported or patients with PPROM were excluded from analysis.…”

Section: Commentmentioning

confidence: 99%

See 2 more Smart Citations

Progesterone inhibits in vitro fetal membrane weakening

Kumar

Springel

Moore

et al. 2015

American Journal of Obstetrics and Gynecology

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Section: Commentmentioning

confidence: 96%

Section: Commentmentioning

confidence: 96%

Section: Commentmentioning

confidence: 99%

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Progesterone inhibits in vitro fetal membrane weakening

Kumar

Springel

Moore

et al. 2015

American Journal of Obstetrics and Gynecology

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“…Protein extract preparation from placental samples, as well as those used in Western blot analyses, were performed as described previously [20]. Immunoblotting was performed with antibodies raised against Bcl-2 (1:1000), Bax (1:1000), cleaved caspase-3 (1:1000), HIF-1a (1:1000), and bactin (1:1000).…”

Section: Western Blot Analysismentioning

confidence: 99%

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

Jiang

Zou

et al. 2015

Biology of Reproduction

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Pre-eclampsia (PE) is a hypertensive disorder that occurs during pregnancy, and is a multifactorial disease. The antiangiogenic factor, soluble fms-like tyrosine kinase 1 (sFlt-1), has been reported to be important in the pathogenesis of PE, but the mechanism of its involvement remains unknown. To test the effects of sFlt-1 on pregnancy, we injected pregnant mice with exogenous mouse sFlt-1. After 18 days of gestation, higher blood pressure, proteinuria, and histological differences were observed compared with controls. Mitochondrial swelling inside the trophoblast cells in the placenta of sFlt-1-treated pregnant mice was observed by electron microscopy, which suggested a role of sFlt-1 in oxidative stress in trophoblasts in PE. Furthermore, apoptosis markers were upregulated in sFlt-1-treated mice. In conclusion, sFlt-1 appears to play a role in oxidative stress, which promotes apoptosis of trophoblasts. This may be an important mechanism in the development of PE.

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“…Steroid hormones are fundamentally important regulators of gestational tissue function including inflammatory reactions. The responsiveness to these hormones varies between tissues and changes during pregnancy, which is partially due to changing steroid hormone receptor levels (Sun et al 1996, Zakar & Hertelendy 2007, Merlino et al 2009, Jiang et al 2012. We have assessed the methylation status of the glucocorticoid receptor (GR, NR3C1), progesterone receptor (PGR, NR3C3) and oestrogen receptor (ESR1, NR3A1) genes in the amnion and decidua to delineate the contribution of receptor gene methylation to the differences in steroid receptor expression levels.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory and steroid receptor gene methylation in the human amnion and decidua

Mitchell¹,

Sykes²,

Pan³

et al. 2013

Journal of Molecular Endocrinology

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Correct timing of parturition requires inflammatory gene activation in the gestational tissues at term and repression during pregnancy. Promoter methylation at CpG dinucleotides represses gene activity; therefore, we examined the possibility that DNA methylation is involved in the regulation of labour-associated genes in human pregnancy. Amnion and decidua were collected at 11-17 weeks of gestation and at term following elective Caesarean delivery or spontaneous labour. Methylation of the inflammatory genes PTGS2, BMP2, NAMPT and CXCL2 was analysed using the Methyl-Profiler PCR System and bisulphite sequencing. Methylation of the glucocorticoid, progesterone and oestrogen receptor genes, involved in the hormonal regulation of gestational tissue function, and the expression of the DNA methyltransferases DNMT1, -3A and -3B were also determined. Variable proportions of inflammatory and steroid receptor gene copies, to a maximum of 50.9%, were densely methylated in both tissues consistent with repression. Densely methylated copy proportions were significantly different between genes showing no relationship with varying expression during pregnancy, between tissues and in individuals. Methylated copy proportions of all genes in amnion and most genes in decidua were highly correlated in individuals. DNMT1 and -3A were expressed in both tissues with significantly higher levels in the amnion at 11-17 weeks than at term. We conclude that the unmethylated portion of gene copies is responsible for the full range of regulated expression in the amnion and decidua during normal pregnancy. Dense methylation of individually variable gene copy proportions happens in the first trimester amnion influenced by sequence context and affected strongly by individual circumstances.

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Tumor necrosis factor (TNF)-α upregulates progesterone receptor-A by activating the NF-κB signaling pathway in human decidua after labor onset

Cited by 16 publications

References 39 publications

Progesterone inhibits in vitro fetal membrane weakening

Progesterone inhibits in vitro fetal membrane weakening

A Role of sFlt-1 in Oxidative Stress and Apoptosis in Human and Mouse Pre-Eclamptic Trophoblasts1

Inflammatory and steroid receptor gene methylation in the human amnion and decidua

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