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Angiopoietin-1, angiopoietin-2 and Tie-2 expression in eutopic endometrium in advanced endometriosis

Title
Angiopoietin-1, angiopoietin-2 and Tie-2 expression in eutopic endometrium in advanced endometriosis
Authors
Hur S.E.Lee J.Y.Moon H.-S.Chung H.W.
Ewha Authors
정혜원문혜성
SCOPUS Author ID
정혜원scopus; 문혜성scopus
Issue Date
2006
Journal Title
Molecular Human Reproduction
ISSN
1360-9947JCR Link
Citation
vol. 12, no. 7, pp. 421 - 426
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Endometriosis is one of the most common gynaecological disorders, but its aetiology and pathogenesis remain obscure. The refluxed menstrual debris in women with endometriosis may be more prone to implantation, invasion and growth in the peritoneum or ovary through the actions of extracellular proteolysis and angiogenesis. It has been hypothesized that the endometrium from women with endometriosis has higher angiogenic activity and expresses more angiogenic factors. Using quantitative competitive PCR (QC-PCR) combined with the reverse transcription of total RNA into cDNA, we investigated the expression of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and Tie-2 in the eutopic endometrium from 56 women with severe endometriosis and that from 64 women without endometriosis during the follicular and luteal cycles. The protein expression from the eutopic endometrium was analysed by western blotting. Results were analysed statistically by Kruskal-Wallis and Mann-Whitney U tests. The eutopic endometrium from women with endometriosis expressed higher levels of mRNA and protein of Ang-1 (P < 0.05) and higher levels of mRNA of Ang-2 than the endometrium from normal women (P < 0.05). Tie-2 mRNA and protein expression from the eutopic endometrium did not differ significantly between endometriosis patients and normal controls. These results suggest that the eutopic endometrium from endometriosis patients is more angiogenic and prone to growth because of greater Ang-1 mRNA and protein expression and higher Ang-2 mRNA expression than the endometrium from women without endometriosis. Thus, increased angiogenic activity may be responsible for the pathogenesis of endometriosis. © 2006 Oxford University Press.
DOI
10.1093/molehr/gal049
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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