TAK1 activation for cytokine synthesis and proliferation of endometriotic cells

Taniguchi, Fuminori; Harada, Tasuku; Miyakoda, Hiroko; Iwabe, Tomio; Deura, Imari; Tagashira, Yukiko; Miyamoto, Ayako; Watanabe, Ayako; Suou, Kana; Uegaki, Takashi; Terakawa, Naoki

doi:10.1016/j.mce.2009.04.012

Cited by 37 publications

(36 citation statements)

References 23 publications

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“…In addition, our results are consistent with the report that TNF ␣ augmented the phosphorylation of TAK1 in endometriotic stromal cells [57] . These results, along with other evidence as reviewed by Guo [3] and with findings reported by other investigators (reviewed in the introduction), strongly suggest the involvement of NF-B in the pathogenesis of endometriosis, and, as such, indicate that NF-B is a promising therapeutic target for treating endometriosis.…”

Section: Discussionsupporting

confidence: 93%

Constitutive and Tumor Necrosis Factor-Alpha-Stimulated Activation of Nuclear Factor-KappaB in Immortalized Endometriotic Cells and Their Suppression by Trichostatin A

Wu¹,

Starzinski‐Powitz

Guo

2010

Gynecol Obstet Invest

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Objective(s): To determine whether nuclear factor-ĸB (NF-ĸB) is constitutively and tumor necrosis factor (TNF)-dependently activated in endometriotic cells, whether trichostatin A (TSA) can suppress NF-ĸB activation and suppress TRAF2/6 and TAK1, and whether TSA and caffeic acid phenyl ester can suppress constitutive and H₂O₂-stimulated proliferation of endometriotic cells. Methods: Two endometriotic cell lines and an endometrial stromal cell line were used as an in vitro model. Electrophoretic mobility shift analysis was used to determine NF-ĸB activation and possible suppression by TSA. Western blot analysis was used to determine whether TSA suppresses phosphorylation of IĸBα, phosphorylation of p65 in the cytoplasm and nuclear translocation, and the expression of TRAF2/6 and TAK1. Results: NF-ĸB was constitutively activated in endometriotic cells, but only minimally in endometrial cells. TNFα stimulation activated NF-ĸB through induction of IĸB phosphorylation, but the activation can be suppressed by TSA. TSA also attenuated constitutive and TNF-dependent p65 phosphorylation and nuclear translocation in endometriotic cells. TRAF2, TRAF6 and TAK1 were constitutively activated and were unaffected by TSA treatment. Conclusions: NF-ĸB activation may play a critical role in the pathogenesis in endometriosis. Targeting NF-ĸB with histone deacetylase inhibitors or other compounds might hold promise as novel therapeutics for endometriosis.

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Section: Discussionsupporting

confidence: 93%

Constitutive and Tumor Necrosis Factor-Alpha-Stimulated Activation of Nuclear Factor-KappaB in Immortalized Endometriotic Cells and Their Suppression by Trichostatin A

Wu¹,

Starzinski‐Powitz

Guo

2010

Gynecol Obstet Invest

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“…Numerous proinflammatory cytokines released by peritoneal macrophages and endometriotic cells are up-regulated by the nuclear factor-kappa B (NF-kB) [18,24]. We demonstrated that the levels of IL-6 and IL-8 increased in the PF of patients with endometriosis [16].…”

Section: Commentsmentioning

confidence: 97%

Effects of low dose oral contraceptive pill containing drospirenone/ethinylestradiol in patients with endometrioma

Taniguchi

Enatsu

Ota

et al. 2015

European Journal of Obstetrics & Gynecology and Reproductiv

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“…Evidence on NF-kB-modulated inflammation in endometriosis has been deduced by studying peritoneal endometriotic implants and peritoneal fluid in vivo, endometriotic epithelial and stromal cells from ovarian endometriotic cysts in vitro, endometriotic cell line cultures, and animal endometriosis models (39,50,(52)(53)(54)(55)(56)(57)(58)(59)(60). Red peritoneal endometriotic implants are characteristically more inflammatory than black endometriotic lesions (10,(61)(62)(63)(64)(65).…”

Section: Nf-kb-modulated Inflammation In Endometriosismentioning

confidence: 99%

“…Other animal studies have shown diminished endometriotic lesion development and cell proliferation in response to NFkB inhibition (71,80,85). In endometriotic cells in culture, inhibition of NF-kB reduced cell proliferation and stimulated apoptosis by down-regulating IL-8, macrophagemigration inhibitory factor, survivin, B-cell lymphoma/leukemia 2 (Bcl-2) and Bcl-XL (antiapoptotic proteins at the mitochondrial level), and by activating caspase 3, caspase 8, and caspase 9 (54,58,59,69,74,75).…”

Section: Nf-kb-regulated Cell Proliferation and Apoptosis In Endometrmentioning

confidence: 99%

Nuclear factor–kappaB: a main regulator of inflammation and cell survival in endometriosis pathophysiology

González-Ramos

Defrère

Devoto

2012

Fertility and Sterility

118

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TAK1 activation for cytokine synthesis and proliferation of endometriotic cells

Cited by 37 publications

References 23 publications

Constitutive and Tumor Necrosis Factor-Alpha-Stimulated Activation of Nuclear Factor-KappaB in Immortalized Endometriotic Cells and Their Suppression by Trichostatin A

Constitutive and Tumor Necrosis Factor-Alpha-Stimulated Activation of Nuclear Factor-KappaB in Immortalized Endometriotic Cells and Their Suppression by Trichostatin A

Effects of low dose oral contraceptive pill containing drospirenone/ethinylestradiol in patients with endometrioma

Nuclear factor–kappaB: a main regulator of inflammation and cell survival in endometriosis pathophysiology

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