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

Khaleque Newaz Khan, Khan KN, Michio Kitajima, Kitajima M, Toshiyuki Imamura, Imamura T, Takehito Imamura, Hiraki K, Koichi Hiraki, Fujishita A, Akira Fujishita, Ichiro Sekine, Sekine I, Tetsuya Ishimaru, Tadayuki Ishimaru, Ishimaru T, Hideaki Masuzaki, Masuzaki H, Hiroaki Masuzaki
Human Reproduction · 2008 · vol. 23(10) , pp. 2210–2219 · doi:10.1093/humrep/den195 · PMID:18596029 · W2088814866
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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 Adult Cell Proliferation Cell Proliferation Cell Proliferation Cytokines Cytokines Cytokines Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endotoxins Endotoxins Endotoxins Enzyme-Linked Immunosorbent Assay

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