Tumor necrosis factor-<b>alpha</b>activates nuclear factor-<b>kappa</b>B but does not regulate progesterone production in cultured human granulosa luteal cells

Gonzalez-Navarrete, Flor; Eisner, Verónica; Morales, Priscilla; Castro, Olga; Pommer, Ricardo; Quiroga, Clara; Lavandero, Sergio; Devoto, Luigi

doi:10.1080/09513590701444839

Cited by 13 publications

(11 citation statements)

References 39 publications

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“…Estrogen receptor (ER) and progesterone receptor (PR) have been found to engage in antagonistic crosstalk with NF-kB, but these interactions are complex and probably cell type-specific (148)(149)(150)(151)(152)(153). Estrogen receptors in ESCs were shown to inhibit DNA binding of p50 and p65 subunits of NF-kB.…”

Section: Nf-kb and Estrogen And Progesterone Receptorsmentioning

confidence: 98%

Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis

González-Ramos

Langendonckt

Defrère

et al. 2010

Fertility and Sterility

Self Cite

150

109

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Section: Nf-kb and Estrogen And Progesterone Receptorsmentioning

confidence: 98%

Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis

González-Ramos

Langendonckt

Defrère

et al. 2010

Fertility and Sterility

Self Cite

150

109

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“…However, in vitro studies have shown that TNF-α may stimulate, inhibit or does not affect steroid hormone secretion in mammal ovarian cells [10]. Polymorphisms in the TNF-α promoter gene may affect transcriptional regulation by modifying the binding site of specific transcription factors [8].…”

Section: Introductionmentioning

confidence: 99%

“…This cytokine regulates numerous cellular processes such as immune and inflammatory responses, differentiation, proliferation and cell death [9]. TNF-α also modulates several biological processes in the mammalian ovary including granulose cell proliferation, follicular development, ovulation and luteolysis, steroidogenesis, prostaglandin and proteoglycan biosynthesis [10].…”

Section: Introductionmentioning

confidence: 99%

TNF-α haplotype association with polycystic ovary syndrome – a South Indian study

Deepika¹,

Reddy²,

Yashwanth³

et al. 2013

J Assist Reprod Genet

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Background Tumor Necrosis Factor Alpha (TNF-α), is a proinflammatory cytokine in the pathogenesis of Polycystic Ovary Syndrome (PCOS). In order to investigate the role of rs1800629 and rs1799964 polymorphisms in relation to anthropometric measures, family history of complex diseases, diet and clinical features, we performed a case control study in PCOS women from South India. Methods A total of 589 samples comprising of 283 patients and 306 controls were enrolled in the present study. Patients were selected based on Rotterdam criteria and ultrasound scanned normal women were selected as controls. Following extraction of DNA, genotyping for rs1800629 and rs1799964 was performed by polymerase chain reaction using tetra primers and PCR-RFLP respectively. Results The distribution of genotypes for rs1799964 was significantly different between the groups (p =0.001), however it was not for rs1800629. Haplotype analysis revealed a significant difference between patients and controls. The predisposing and protective role of haplotype with mutant allele at both loci (combination 3) and haplotype with mutant allele at either loci was reflected by the over representation of combination 3 in patients and combination 2 in controls respectively. In addition, rs1799964 showed an association with dietary habit, clinical hyperandrogenism and AAO. The modifying role of TT genotype on age at onset was noted in quartile analysis. ConclusionReplicative studies on the influence of TNF-α polymorphism in different ethnic groups may identify the potentiality of these polymorphisms as markers of inflammation and in turn may help the clinicians for the better management of the condition.

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“…In this sense, the NFkB mRNA expression was increased in the PCO ovary after incubation with the PCO MO secretions. It is known that the activation of this transcription factor, which induces the transcription of downstream target genes involved in the inflammatory and apoptotic process (Perkins 2007), is induced by TNF in rat granulosa cells through phosphorylation of IkB (Gonzalez-Navarrete et al 2007). Considering the proapoptotic role for TNF in reproductive tissues (Kaipia et al 1996, Hussein 2005, Haider & Knofler 2009) and having observed that secretions from spleen MO of PCO rats contain more TNF than secretions from control MO (Figueroa et al 2012), the induction of NFkB mRNA expression in the PCO ovary after incubation with control MO secretions, which was even more accentuated with PCO MO secretions, could be associated, at least to some extent, to the TNF levels of the MO secretions.…”

Section: Discussionmentioning

confidence: 99%

Role of macrophage secretions on rat polycystic ovary: its effect on apoptosis

et al. 2015

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Polycystic ovarian syndrome is the most common endocrine disorder among women of reproductive age. Little is known about its etiology, although the evidence suggests an intrinsic ovarian abnormality in which endocrine, metabolic, neural and immune factors would be involved. In this work, the effects of macrophage (MO) secretion on ovarian apoptosis in a polycystic ovary syndrome rat model (PCO rat) induced by estradiol valerate are studied. Spleen MO secretions were used to stimulate ovaries and ovarian interstitial and granulosa cells from both PCO and control rats. Ovarian hormones and prostaglandin E 2 (PGE 2 ) were measured by RIA; ovarian mRNA levels of Bax, Bcl2 and NFkB by RT-PCR; and ovarian inducible nitric oxide synthase (iNOS) by western blot. The number of apoptotic cells was evaluated by TUNEL. In the PCO ovary, the MO secretions from PCO rats increased the Bax and NFkB mRNA expressions and increased TUNEL staining in both granulosa and theca cells. In addition, the PCO MO secretions produced a decrease of nitric oxide release, iNOS protein level and PGE 2 content in the PCO ovary, and it also induced an increase of androstenedione production by PCO interstitial cells, in comparison with control MO secretions. Considering these results and knowing that testosterone stimulates tumour necrosis factor-a production by PCO MO modifying ovarian response by increasing androstenedione, it is reasonable to suggest that the increase of androgens stimulated in ovarian cells by PCO MO secretions could in turn stimulate the cytokine production from MO, thus maintaining an apoptotic vicious cycle in the PCO ovary.Reproduction (2015) 150 437-448

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Tumor necrosis factor-alphaactivates nuclear factor-kappaB but does not regulate progesterone production in cultured human granulosa luteal cells

Cited by 13 publications

References 39 publications

Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis

Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis

TNF-α haplotype association with polycystic ovary syndrome – a South Indian study

Role of macrophage secretions on rat polycystic ovary: its effect on apoptosis

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