TAK1 activation for cytokine synthesis and proliferation of endometriotic cells

Fuminori Taniguchi, Taniguchi F, Tasuku Harada, Harada T, Miyakoda H, Hiroko Miyakoda, Tomio Iwabe, Iwabe T, Deura I, Imari Deura, Yukiko Tagashira, Tagashira Y, Ayako Miyamoto, Miyamoto A, Ayako Watanabe, Watanabe A, Kana Suou, Suou K, Takashi Uegaki, Uegaki T, Terakawa N, Naoki Terakawa
Molecular and cellular endocrinology · 2009 · vol. 307(1-2) , pp. 196–204 · doi:10.1016/j.mce.2009.04.012 · PMID:19410630 · W2035431497
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This study investigated the role of TAK1 activation in mediating cytokine synthesis and cell proliferation within endometriotic cells.

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Abstract

Endometriosis causes pelvic pain and infertility in women of reproductive age. We explored TNFalpha-induced specific signaling pathways and gene expressions in endometriotic stromal cells (ESCs). Based on the data of the pathway specific cDNA array, we analyzed the role of TAK1, which is believed to work as a common mediator for NF-kappaB and MAPK pathways. Using the NF-kappaB pathway array, we found that TNFalpha upregulated ICAM-3, IL-6, IL-8, TAK1, JNK2, RelA, and TLR4 expressions. TNFalpha augmented the phosphorylation of TAK1. By transfection of TAK1 siRNA, TNFalpha-induced phosphorylation of IkappaBalpha, JNK1/2, and p38MAPK, as well as IL-6 or IL-8 expression, were repressed. TAK1 silencing in TNFalpha-pretreated ESCs caused a decrease in the proportion of cells in S-phase, and reduced TNFalpha-promoted BrdU incorporation. We provide the first evidence that TNFalpha and its downstream TAK1, which are key mediators for NF-kappaB and MAPK pathways, may be involved in the pathogenesis of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Cytokines Endometriosis Endometriosis MAP Kinase Kinase Kinases Cell Proliferation Cell Proliferation Cytokines DNA, Complementary Endometriosis Enzyme Activation Enzyme Activation Female Gene Expression Regulation Gene Expression Regulation Gene Silencing Gene Silencing Humans Interleukin-6 Interleukin-6 Interleukin-8

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (30)

Cited by (24)

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License: CC0 · commercial use OK