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Interleukin-1β induces cyclooxygenase-2 expression and promotes the invasive ability of human mesenchymal stem cells derived from ovarian endometrioma.

Abstract：

OBJECTIVE:To elucidate the role of interleukin-1β (IL-1β) on cyclooxygenase-2 (COX-2) expression and invasion of endometrioma-derived ectopic endometrial mesenchymal stem cells (EN-MSCs) and to develop an organoid method to study the invasive ability of endometrial cells. DESIGN:Gene expression and cell functions. SETTING:Kaohsiung Medical University, Kaohsiung, Taiwan. PATIENT(S):Human eutopic and endometrioma-derived ectopic EN-MSCs were isolated from different endometrium biopsy samples after surgery for treatment of endometriosis. INTERVENTION(S):Chemical treatment of cell culture. MAIN OUTCOME MEASURE(S):Comparative analysis of genomewide messenger RNA (mRNA) expression, cell migration, and invasion abilities in cell culture and organoid culture. RESULT(S):Gene expression profiles revealed that the expression of IL-1β and COX-2 were statistically significantly higher in ectopic EN-MSCs compared with eutopic EN-MSCs. These enhanced expressions coincided with a greater ability for cell migration and invasion in ectopic EN-MSCs and were found to be distinctly regulated by IL-1β which up-regulates COX-2 expression. Furthermore, IL-1β treatment of ectopic EN-MSCs in organoids was found to induce tentacle-like structures that mimicked cell invasion. CONCLUSION(S):These results indicate that COX-2 and IL-1β regulate the invasion ability of ectopic EN-MSCs. The information may be useful for developing a new therapeutic strategy for endometriosis. The ex vivo invasion model will be useful for characterization of EN-MSCs.

journal_name

Fertil Steril

journal_title

Fertility and sterility

authors

Kao AP,Wang KH,Long CY,Chai CY,Tsai CF,Hsieh TH,Hsu CY,Chang CC,Lee JN,Tsai EM

doi

10.1016/j.fertnstert.2011.06.041

subject

Has Abstract

pub_date

2011-09-01 00:00:00

pages

678-684.e1

issue

3

eissn

0015-0282

issn

1556-5653

pii

S0015-0282(11)01018-1

journal_volume

96

pub_type

杂志文章

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