Retinoic acid suppresses growth of lesions, inhibits peritoneal cytokine secretion, and promotes macrophage differentiation in an immunocompetent mouse model of endometriosis

Retinoic acid inhibition of endometriotic-implant development in mouse model endometriosis may be related to suppression of interleukin-6 and macrophage chemotactic factor-1 production, and promotion of peritoneal macrophage differentiation.

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Authors

Friedrich Wieser, M.D., Juanjuan Wu, M.D., Ph.D., Zhaoju Shen, Ph.D., Robert N. Taylor, M.D., Ph.D., Neil Sidell, Ph.D.

Vol 97, Issue 6 , Pages 1430-1437

Abstract

Objective:

To determine the effects of all-trans-retinoic acid (RA) on establishment and growth of endometrial lesions, peritoneal interleukin-6 (IL-6) and macrophage chemotactic factor-1 (MCP-1) concentrations, and CD38, CD11b, and F4/80 expression on peritoneal macrophages in an immunocompetent mouse model of endometriosis.

Design:

Experimental transplantation study using mice.

Setting:

Academic medical center.

Animal(s):

C57BL/6 recipient mice and syngeneic green fluorescent protein transgenic (GFP+) mice.

Intervention(s):

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).

Main Outcome Measure(s):

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, and expression of CD11b, F4/80, and CD38 on peritoneal macrophages.

Result(s):

Retinoic acid treatment for 17 days reduced the number of implants versus controls and decreased the frequency of lesions with vessels. Peritoneal washings in RA-treated animals had lower concentrations of 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 versus controls.

Conclusion(s):

The development of endometriotic implants is inhibited by RA. This effect may be caused, at least in part, by reduced IL-6 and MCP-1 production and enhanced differentiation of peritoneal macrophages.

Read the full text at: http://www.fertstert.org/article/S0015-0282(12)00318-4/fulltext


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Fertility and Sterility® is an international journal for obstetricians, gynecologists, reproductive endocrinologists, urologists, basic scientists and others who treat and investigate problems of infertility and human reproductive disorders. The journal publishes juried original scientific articles in clinical and laboratory research relevant to reproductive endocrinology, urology, andrology, physiology, immunology, genetics, contraception, and menopause. Fertility and Sterility® encourages and supports meaningful basic and clinical research, and facilitates and promotes excellence in professional education, in the field of reproductive medicine.

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