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

Oleh:

Sotnikova, Natalia Yu ; Antsiferova, Yulia S. ; Posiseeva, Lyubov V.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 93 no. 08 (Jun. 2010), page 2701-2705.
Topik: Endometriosis; rat model; endometrium; invasiveness; MMP-2; TIMP-2; TGFß2; cytokines

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2010.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To compare the expression of MMP-2, TIMP-2, and TGFß2 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, TGFß2 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 TGFß2 mRNA expression was seen at the 14th day postsurgery. In humans, elevation of TIMP-2 mRNA expression in eutopic endometrium and of MMP-2, TGFß2 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 TGFß2 mRNA expression in endometrium of healthy women. Conclusion(s) Supposedly MMP–TIMP balance is important in promoting endometriotic tissue invasion and TGFß2 in regulating ectopic endometrium growth.

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