Regulation of miR-33b on endometriosis and expression of related factors

Endometriosis is a common benign disease in gynecology, and can cause chronic pelvic pain, dysmenorrhea and even infertility. Its pathogenesis mechanism has not been fully illustrated. miRNA (miR) participates in various biological activities including cell growth, proliferation, apoptosis, organ formation, inflammation and tumor. Its role in endometriosis has not been reported. MiR-33b is involved in cell metabolism, proliferation and invasion, but with its function and mechanism in endometriosis unknown.

Real-time PCR was used to test miR-33b expression in ectopic endometrial and normal tissues. In vitro cultured endometrial cells were transfected with miR-33b mimic or inhibitor, followed by Real-time PCR for miR-33b expression. MTT method detected endometrial cell proliferation. Caspase 3 activity was quantified by test kit. Real-time PCR and Western blot measured effect of miR-33b on vascular endothelial growth factor (VEGF) and matrix metalloprotein 9 (MMP-9).

MiR-33b was down-regulated in ectopic endometrial tissues (p < 0.05 compared to normal tissues). Transfection of miR-33b inhibitor facilitated endometrial proliferation, decreased Caspase 3 activity, increased VEGF and MMP-9 mRNA or protein expression (p < 0.05 compared to control group). MiR-33b mimic suppressed endometrial proliferation, elevated Caspase 3 activity, and decreased VEGF or MMP-9 expression (p < 0.05 compared to control group).

MiR-33b can mediate cell apoptosis, alter VEGF and MMP-9 expression and affect proliferation and apoptosis of uterus endometrial cells, thus participating endometriosis formation.