title: Retinoic acid suppresses growth of lesions, inhibits peritoneal cytokine secretion, and promotes macrophage differentiation in an immunocompetent mouse model of endometriosis.
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.
  
  
  METHODS
  Experimental transplantation study using mice.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  C57BL/6 recipient mice and syngeneic green fluorescent protein transgenic (GFP+) mice.
  
  
  METHODS
  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).
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
authors.forename: Friedrich
authors.initials: F
authors.lastname: Wieser
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Wu
authors.forename: Zhaoju
authors.initials: Z
authors.lastname: Shen
authors.forename: Robert N
authors.initials: RN
authors.lastname: Taylor
authors.forename: Neil
authors.initials: N
authors.lastname: Sidell
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D018932:Chemokine CCL2 / Q000378:metabolism*; D004195:Disease Models, Animal; D004715:Endometriosis / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D005260:Female; D049452:Green Fluorescent Proteins / Q000235:genetics; D007121:Immunocompetence; D015850:Interleukin-6 / Q000378:metabolism*; D008264:Macrophages / Q000166:cytology* / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010537:Peritoneum / Q000378:metabolism*; D019737:Transplants / Q000009:adverse effects; D014212:Tretinoin / Q000494:pharmacology*; D014599:Uterus / Q000166:cytology
chemical_list: D000970:Antineoplastic Agents; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D015850:Interleukin-6; D049452:Green Fluorescent Proteins; D014212:Tretinoin