Retinoic acid suppresses growth of lesions, inhibits peritoneal cytokine secretion, and promotes macrophage differentiation in an immunocompetent mouse model of endometriosis.
Retinoic acid suppresses growth of lesions, inhibits peritoneal cytokine secretion, and promotes macrophage differentiation in an immunocompetent mouse model of endometriosis.
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DOI：
10.1016/j.fertnstert.2012.03.004
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发表时间：
2012-06
影响因子：
6.7
通讯作者：
Sidell, Neil
中科院分区：
文献类型：
--
作者：
Wieser, Friedrich;Wu, Juanjuan;Shen, Zhaoju;Taylor, Robert N.;Sidell, Neil
To determine the effects of retinoic acid (RA) on establishment and growth of endometrial lesions, peritoneal IL-6 and MCP-1 concentrations, and CD38, CD11b, F4/80 expression on peritoneal macrophages in an immunocompetent mouse model of endometriosis. Experimental transplantation study using mice. Academic medical center. C57BL/6 recipient mice and syngeneic Green Fluorescent Protein transgenic (GFP+) mice. Recipient mice were inoculated with GFP+ minced uterine tissue to induce endometriosis and treated with RA (400 nmol/day) or vehicle for 17 days (3 days before to 14 days after tissue injection). Total number of GFP+ implants in recipient mice, number of implants showing visible blood vessels, total volume of established lesions per mouse, concentrations of IL-6 and MCP-1 in peritoneal fluid, expression of CD11b, F4/80 and CD38 on peritoneal macrophages. 17 days of RA treatment reduced the number of implants versus controls and decreased the frequency of lesions with vessels. Peritoneal washings in RA-treated animals had lower IL-6 and MCP-1 than controls 3 days after endometrial inoculation and lower levels of IL-6 on day 14 after inoculation. Concomitant with these effects on day 14, CD38, CD11b, and F4/80 were higher on macrophages from RA-treated mice vs. controls. RA inhibits the development of endometriotic implants. This effect may be caused, at least in part, by reduced IL-6 and MCP-1 production and enhanced differentiation of peritoneal macrophages.
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