Mechanisms regulating invasiveness and growth of endometriosis lesions in rat experimental model and in humans

Fertil Steril. 2010 May 15;93(8):2701-5. doi: 10.1016/j.fertnstert.2009.11.024. Epub 2010 Jan 8.

Abstract

Objective: To compare the expression of MMP-2, TIMP-2, and TGFbeta2 mRNA in experimental and human endometriotic lesions and to assess the possibility of its cytokine regulation.

Design: Experimental laboratory study.

Setting: Medical center. ANIMALS AND PATIENT(S): Thirty female Wistar rats, 17 women with endometriosis, 11 healthy women.

Intervention(s): Uterine transplants were attached to rat peritoneum via the surgical autotransplantation technique. The collection of endometriotic implants at 7, 14, and 21 days postsurgery and laparoscopic collection of peritoneal fluid, ectopic, and matched eutopic endometrium from women with endometriosis were performed.

Main outcome measure(s): MMP-2, TIMP-2, TGFbeta2 mRNA expression in endometrium was assessed by real-time reverse-transcription polymerase chain reaction.

Result(s): In rats, the increase of MMP-2 and decrease of TIMP-2 mRNA expression was noted at the 7th day, and an increase of TGFbeta2 mRNA expression was seen at the 14th day postsurgery. In humans, elevation of TIMP-2 mRNA expression in eutopic endometrium and of MMP-2, TGFbeta2 mRNA expression in ectopic endometrium was observed. Autologous peritoneal fluid stimulated MMP-2 mRNA expression in eutopic endometrium of women with endometriosis. Cytokines derived from ectopic lesions mononuclear cells increased TGFbeta2 mRNA expression in endometrium of healthy women.

Conclusion(s): Supposedly MMP-TIMP balance is important in promoting endometriotic tissue invasion and TGFbeta2 in regulating ectopic endometrium growth.

MeSH terms

  • Adult
  • Animals
  • Ascitic Fluid / physiology
  • Disease Models, Animal
  • Endometriosis / etiology
  • Endometriosis / metabolism*
  • Endometrium / metabolism*
  • Female
  • Humans
  • Matrix Metalloproteinase 2 / biosynthesis*
  • Matrix Metalloproteinase 2 / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Tissue Inhibitor of Metalloproteinase-2 / biosynthesis*
  • Tissue Inhibitor of Metalloproteinase-2 / genetics
  • Transforming Growth Factor beta2 / biosynthesis*
  • Transforming Growth Factor beta2 / genetics

Substances

  • RNA, Messenger
  • Transforming Growth Factor beta2
  • Tissue Inhibitor of Metalloproteinase-2
  • Matrix Metalloproteinase 2