Toll-like receptor 4-mediated growth of endometriosis by human heat-shock protein 70

Khaleque Newaz Khan, Michio Kitajima, Toshiyuki Imamura, Takehito Imamura, Koichi Hiraki, Akira Fujishita, Ichiro Sekine, Tadayuki Ishimaru, Tetsuya Ishimaru, Hiroaki Masuzaki, Hideaki Masuzaki
Human Reproduction · 2008 · vol. 23(10) , pp. 2210–2219 · doi:10.1093/humrep/den195 · PMID:18596029 · W2088814866
article OA: bronze CC0 ⤵ 37 in-corpus citations
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Human heat-shock protein 70 promotes endometriosis growth via Toll-like receptor 4 by stimulating cytokine production and endometrial stromal cell proliferation.

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Abstract

BACKGROUND: We investigated the role of human heat-shock protein 70 (Hsp70) in Toll-like receptor 4 (TLR4)-mediated growth of endometriosis. METHODS: TLR4 expression was examined in macrophages (M) isolated in primary culture from the peritoneal fluid of women with and without endometriosis. The production of a number of macromolecules by non-treated M, Hsp70-treated M and after treatment with anti-TLR4 antibody was examined by enzyme linked immunosorbent assay (ELISA). The single and combined effects of Hsp70 and lipopolysaccharide (LPS) on the growth of endometrial stromal cells were analyzed by 5-bromo-2-deoxyuridine (BrdU) incorporation study. Hsp70 levels in eutopic and ectopic endometria were measured by ELISA. RESULTS: TLR4 was detected in isolated M at protein and gene level. Hsp70 (10 microg/ml) significantly stimulated the production of hepatocyte growth factor, vascular endothelial cell growth factor, interleukin-6 and tumor necrosis factor alpha by M derived from women with endometriosis compared with M derived from women with no endometriosis (P < 0.05 for each). This effect of Hsp70 was abrogated after pretreatment of M with anti-TLR4 antibody. BrdU incorporation indicated that Hsp70 significantly enhanced the growth of endometrial stromal cells ( approximately 50% increase) from women with endometriosis compared to non-treated cells. A synergistic effect on cell proliferation was observed between exogenous Hsp70 and LPS and this was significantly suppressed by pretreatment of cells with anti-TLR4 antibody (P < 0.05). Tissue levels of Hsp70 were significantly higher in the eutopic endometria (P < 0.05) and opaque red lesions (P < 0.01) derived from women with endometriosis than from other peritoneal lesions or from women with no endometriosis. CONCLUSIONS: A prominent stress reaction was observed in blood-filled opaque red peritoneal lesions. Human Hsp70 induces pelvic inflammation and may be involved in TLR4-mediated growth of endometrial cells derived from women with endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis HSP70 Heat-Shock Proteins Toll-Like Receptor 4 Adult Cell Proliferation Cell Proliferation Cytokines Cytokines Endometriosis Endometriosis Endometrium Endotoxins Endotoxins Enzyme-Linked Immunosorbent Assay Female Gene Expression Regulation Hepatocyte Growth Factor Hepatocyte Growth Factor Hepatocyte Growth Factor HSP70 Heat-Shock Proteins

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