Indoleamine 2,3-dioxygenase-1 (IDO1) enhances survival and invasiveness of endometrial stromal cells via the activation of JNK signaling pathway.

Jie Mei, Ming‐Qing Li, Ming-Qing Li, Ding Ding, Da-Jin Li, Da‐Jin Li, Liping Jin, Li-Ping Jin, Wei-Guo Hu, Weiguo Hu, Xiao-Yong Zhu, Xiao‐Yong Zhu
International journal of clinical and experimental pathology · 2013 · vol. 6(3) , pp. 431–44 · PMID:23411497 · PMC3563200 · W156853574
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Indoleamine 2,3-dioxygenase-1 (IDO1) overexpression in endometrial stromal cells increases their survival and invasiveness by activating the JNK signaling pathway.

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Abstract

Evidence for an immunosuppressive function of indoleamine 2,3-dioxygenase (IDO) has been accumulating. However, the unusual distribution of IDO1 in gynecologic cancer cells suggests that modulating immunity may not its only function. To clarify the physiological importance of IDO1 in endometriosis, a tumor-like benign disease, we have investigated the potential mechanism by which IDO1 modulated endometrial stromal cells (ESCs) proliferation and invasion. ESCs were obtained from 16 control women (normal) and 14 patients with ovarian endometrioma, then the normal ESCs were treated with plasmid pEGFP-N1-IDO1 or SD11-IDO1 short hairpin RNA (shRNA) alone, or in combination with c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and subjected to cell viability, proliferation, apoptosis assay and Matrigel invasion assay. IDO1 mRNA expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction (real-time PCR), and protein levels of IDO1, survivin, protein 53 (p53), matrix metalloproteinase (MMP)-2, MMP-9, tissue-inhibitor of metalloproteinase-1 (TIMP-1) and cyclooxygenase-2 (COX-2) in IDO1-overexpressing and IDO1-deficiency ESCs were analyzed by in-cell Western. We found that IDO1 expression was higher in endometriosis-derived eutopic and ectopic ESCs, compared with endometriosis-free normal ESCs. As a result, IDO1-overexpression in ESCs was markedly linked to reduction of apoptosis and p53 expression, and upregulation of survival, proliferation, invasion, as well as expression of MMP-9, COX-2 expression, rather than expression of survivin, MMP-2 and TIMP-1. Reversely, JNK blockage could abrogate these alterations of ESCs in IDO1-overexpressing milieu, suggesting that JNK signaling pathway was indispensable for ESCs survival, proliferation and invasion enhanced by IDO1, which may contribute to the pathophysiology of endometriosis.

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Condition tags

endometriosisendometrioma

MeSH descriptors

Endometriosis Endometrium Indoleamine-Pyrrole 2,3,-Dioxygenase MAP Kinase Signaling System Stromal Cells Uterine Diseases Adult Anthracenes Anthracenes Apoptosis Apoptosis Apoptosis Cell Movement Cell Movement Cell Proliferation Cell Proliferation Cell Survival Cell Survival Cell Survival Endometriosis

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