Role of miR‑449b‑3p in endometriosis via effects on endometrial stromal cell proliferation and angiogenesis

Mol Med Rep. 2018 Sep;18(3):3359-3365. doi: 10.3892/mmr.2018.9341. Epub 2018 Jul 31.

Abstract

Endometriosis is a common gynecological disease and the pathogenesis is not clearly understood. Previous studies have demonstrated via microarray techniques that microRNA (miR)‑449b was significantly downregulated both in ectopic and eutopic endometrium in patients with endometriosis. In the present study, the aberrant expression of miR‑449b was further confirmed by reverse transcription‑quantitative polymerase chain reaction. It was demonstrated that miR‑449b‑3p was downregulated in ectopic and eutopic tissues from women with endometriosis, and the same expression pattern was observed in endometrial stromal cells (ESCs) of eutopic endometrium from women with endometriosis and normal endometrium from women without endometriosis. Functional analysis, including an MTT assay, apoptosis conducted by flow cytometry, capillary‑like tube formation assay and invasion assay, indicated that the upregulated expression of miR‑449b‑3p inhibited the proliferation of ESCs and that the supernatants of miR‑449b‑overexpressing ESCs inhibited the formation of tubular structures in human umbilical vein endothelial cells, whereas it has no effect on ESC apoptosis and invasiveness. These results suggest that the aberrant expression of miR‑449b‑3p was involved in the development and progression of endometriosis.

MeSH terms

  • Adult
  • Apoptosis / genetics
  • Case-Control Studies
  • Cell Movement / genetics
  • Cell Proliferation
  • Cell Survival / genetics
  • Cells, Cultured
  • Endometriosis / genetics*
  • Endometriosis / pathology*
  • Endothelial Cells / metabolism
  • Female
  • Genetic Vectors / genetics
  • Humans
  • Lentivirus / genetics
  • MicroRNAs / genetics*
  • Neovascularization, Pathologic / genetics*
  • Stromal Cells / metabolism*
  • Transduction, Genetic

Substances

  • MIRN449 microRNA, human
  • MicroRNAs