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Reports from Nagasaki University describe recent advances in endometriosis.
According to recent research from Sakamoto, Japan, "We investigated the role of human heat-shock protein 70 (Hsp70) in Toll-like receptor 4 (TLR4)-mediated growth of endometriosis. TLR4 expression was examined in macrophages (M phi) 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 phi, Hsp70-treated M phi 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. TLR4 was detected in isolated M phi at protein and gene level. Hsp70 (10 mu g/ml) significantly stimulated the production of hepatocyte growth factor, vascular endothelial cell growth factor, interleukin-6 and tumor necrosis factor alpha by M phi derived from women with endometriosis compared with M phi derived from women with no endometriosis (P
The researchers concluded: "Human Hsp70 induces pelvic inflammation and may be involved in TLR4-mediated growth of endometrial cells derived from women with endometriosis."
Khan and colleagues published their study in Human Reproduction (Toll-like receptor 4-mediated growth of endometriosis by human heat-shock protein 70. Human Reproduction, ...
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Source: HighBeam Research, Reports from Nagasaki University describe recent advances in...