Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Chi-Jr Liao, Pei-Tzu Li, Pei‐Tzu Li, Ying-Chu Lee, Sheng-Hsiang Li, Sheng‐Hsiang Li, Sin Tak Chu
Reproduction (Cambridge, England) · 2013 · vol. 147(2) , pp. 179–187 · doi:10.1530/rep-13-0236 · PMID:24194573 · W2172161620
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Lipocalin 2 induces epithelial-mesenchymal transition in stressed endometrial cells, promoting migration and invasion, which may correlate with endometriosis development in mice.

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Abstract

Lipocalin 2 (LCN2) is an induced stressor that promotes the epithelial-mesenchymal transition (EMT). We previously demonstrated that the development of endometriosis in mice correlates with the secretion of LCN2 in the uterus. Here, we sought to clarify the relationship between LCN2 and EMT in endometrial epithelial cells and to determine whether LCN2 plays a role in endometriosis. Antibodies that functionally inhibit LCN2 slowed the growth of ectopic endometrial tissue in a mouse model of endometriosis, suggesting that LCN2 promotes the formation of endometriotic lesions. Using nutrient deprivation as a stressor, LCN2 expression was induced in cultured primary endometrial epithelial cells. As LCN2 levels increased, the cells transitioned from a round to a spindle-like morphology and dispersed. Immunochemical analyses revealed decreased levels of cytokeratin and increased levels of fibronectin in these endometrial cells, adhesive changes that correlate with induction of cell migration and invasion. Lcn2 knockdown also indicated that LCN2 promotes EMT and migration of endometrial epithelial cells. Our results suggest that stressful cellular microenvironments cause uterine tissues to secrete LCN2 and that this results in EMT of endometrial epithelial cells, which may correlate with the development of ectopic endometriosis. These findings shed light on the role of LCN2 in the pathology of endometrial disorders.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Acute-Phase Proteins Endometriosis Endometrium Epithelial Cells Epithelial-Mesenchymal Transition Lipocalins Oncogene Proteins Acute-Phase Proteins Acute-Phase Proteins Acute-Phase Proteins Animals Antibodies Antibodies Cell Movement Cell Movement Cells, Cultured Disease Models, Animal Endometriosis Endometrium Endometrium

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