miRNA ‐199a‐5p regulates VEGFA in endometrial mesenchymal stem cells and contributes to the pathogenesis of endometriosis

Chia-Yi Hsu, Chia‐Yi Hsu, Tsung‐Hua Hsieh, Tsung-Hua Hsieh, Cheng-Fang Tsai, Cheng‐Fang Tsai, Hung‐Pei Tsai, Hung-Pei Tsai, Hung‐Sheng Chen, Hung-Sheng Chen, Yu Chang, Hui‐Yu Chuang, Hui-Yu Chuang, Jau-Nan Lee, Ya-Ling Hsu, Ya‐Ling Hsu, Eing‐Mei Tsai, Eing-Mei Tsai
The Journal of Pathology · 2013 · vol. 232(3) , pp. 330–343 · doi:10.1002/path.4295 · PMID:24155090 · W2141821852
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This study found that miRNA-199a-5p targets VEGFA to regulate proliferation, motility, and angiogenesis in endometrial mesenchymal stem cells and reduces endometriotic lesion size in vivo.

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Abstract

It is believed that endometrial miRNAs contribute to the aetiology of endometriosis in stem cells; however, the mechanisms remain unclear. Here we collected serum samples from patients with or without endometriosis and characterized the miRNA expression profiles of these two groups. MicroRNA-199a-5p (miR-199a-5p) was dramatically down-regulated in patients with endometriosis compared with control patients. In addition, we found that the tumour suppressor gene, SMAD4, could elevate miR-199a-5p expression in ectopic endometrial mesenchymal stem cells. Up-regulation of miR-199a-5p suppressed cell proliferation, motility and angiogenesis of these ectopic stem cells by targeting the 3' untranslated region of VEGFA. Furthermore, we established an animal model of endometriosis and found that miR-199a-5p could decrease the size of endometriotic lesions in vivo. Taken together, this newly identified miR-199a-5p module provides a new avenue to the understanding of the processes of endometriosis development, especially proliferation, motility and angiogenesis, and may facilitate the development of potential therapeutics against endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometrium Mesenchymal Stem Cells MicroRNAs Vascular Endothelial Growth Factor A Adult Animals Chromatin Immunoprecipitation Disease Models, Animal Endometriosis Endometriosis Endometrium Female Humans Immunohistochemistry In Situ Hybridization Mesenchymal Stem Cells Mice Mice, Inbred C57BL Mice, Nude

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