Literature DB >> 15088640

Macrophages are activated by 17beta-estradiol: possible permission role in endometriosis.

Min Hong1, Quan Zhu.   

Abstract

On the basis of the common occurrence of high concentration of estrogen and activated macrophages in patients with endometriosis, we postulate that interaction between 17beta-estradiol and macrophage may be an important affair in endometriosis. So our study was focused on the effect of 17beta-estradiol on macrophage. First morphology of macrophages was examined with environmental scanning electron microscopy. Increased size, extension of more microvilli, expression of retraction fibers and elaboration of membrane ruffles were detected in 17beta-estradiol treated macrophages. Then Nitrate and nitrite level in the supernatant was measured by the method of Griess and iNOS expression was analyzed using immunohistochemical staining. It showed that 17beta-estradiol could induce NO release from peritoneal macrophages and expression of iNOS was increased. Also more TNF-alpha in supernatant that was measured by MTT via L929 cell was produced by macrophages under the inducing of 17beta-estradiol. Furthermore, [Ca2+]i, which was viewed by microscope in a laser scanning confocal unit, elevated 39.8% in peritoneal macrophages after 17beta-estradiol 100 nmol/L treated. The results above demonstrated that peritoneal macrophage had been activated in both morphology and cytokine line when interaction with 17beta-estradiol, which indicated that macrophage activated by 17beta-estradiol might play a permission role in development of endometriosis.

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Year:  2004        PMID: 15088640     DOI: 10.1078/0940-2993-00335

Source DB:  PubMed          Journal:  Exp Toxicol Pathol        ISSN: 0940-2993


  5 in total

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5.  Expression and function of Toll-like receptor 4 in the endometrial cells of the uterus.

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  5 in total

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