Interleukin-4 induces expression of eotaxin in endometriotic stromal cells

Zhuo Ouyang, Ouyang Z, Yutaka Osuga, Osuga Y, Yasushi Hirota, Tetsuya Hirata, Osamu Yoshino, Yoshino O, Kaori Koga, Yano T, Tetsu Yano, Yuji Taketani, Taketani Y
Fertility and sterility · 2009 · vol. 94(1) , pp. 58–62 · doi:10.1016/j.fertnstert.2009.01.129 · PMID:19338989 · W1998409306
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This paper investigated how interleukin-4 affects endometriotic stromal cells, finding that it increases the expression of eotaxin.

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Abstract

ObjectiveTo study the relationship between eotaxin and interleukin-4 (IL-4) in the pathophysiology of endometriosis.DesignComparative and laboratory study.SettingUniversity teaching hospital reproductive endocrinology and infertility practice.Patient(s)Ectopic endometrial tissues were collected from women with endometriosis.Intervention(s)Ectopic endometrial stromal cells (ESCs) were isolated and cultured with IL-4. Ectopic endometriotic tissues were immunostained for eotaxin and IL-4.Main outcome measure(s)Gene expression of eotaxin was determined by standard and real-time reverse-transcriptase polymerase chain reaction. Secretion of eotaxin from ESC was measured using specific ELISA. The immunostained sections were examined.Result(s)Interleukin-4 (IL-4) increased mRNA expression and protein secretion of eotaxin from ESC in a dose-dependent manner. Immunohistochemical analysis showed that eotaxin-positive cells colocalized with IL-4-positive cells and accumulated around the blood vessels in the stroma of endometriotic tissue.Conclusion(s)IL-4 induces eotaxin in ESCs, which might promote angiogenesis and the subsequent development of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Chemokine CCL11 Endometriosis Gene Expression Regulation Interleukin-4 Animals Chemokine CCL11 Chemokine CCL11 Chemokine CCL11 Endometriosis Endometriosis Female Humans Interleukin-4 Mice Neovascularization, Pathologic Neovascularization, Pathologic Neovascularization, Pathologic Stromal Cells Stromal Cells

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