Macrophages are activated by 17b-estradiol: possible permission role in endometriosis
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This study investigated the activation of macrophages by 17b-estradiol and its potential role in endometriosis.
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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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Cited by (9)
- Overview and Updates on the Role of Genetic Variants in Endometriosis Susceptibility and Pathogenesis 2026
- Endometriosis-associated Pain: Mechanism, Neuroimmune Signature, and Translational Precision Strategies 2026
- Immune pathway through endometriosis to ovarian cancer 2024
- Immune and endocrine regulation in endometriosis: what we know 2023
- Protective effect of cabergoline on mitochondrial oxidative stress-induced apoptosis is mediated by modulations of TRPM2 in neutrophils of patients with endometriosis 2020
- Dysfunctional signaling underlying endometriosis: current state of knowledge 2018
- Aromatase and endometriosis: estrogens play a role 2014
- ERB-041, a selective ERβ agonist, inhibits iNOS production in LPS-activated peritoneal macrophages of endometriosis via suppression of NF-κB activation 2009
- Combination of estrogen and dioxin is involved in the pathogenesis of endometriosis by promoting chemokine secretion and invasion of endometrial stromal cells 2008
Source provenance
- europepmc
- last seen: 2026-09-17T06:16:55.786923+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-05-13T22:12:38.158000+00:00
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