Figure 2.

Overexpression of miR-26b-5p suppresses the increase of COX-2 expression and PGE₂ release but prevents the decrease of PGI₂ release induced by CoCl₂ in placental trophoblasts. (A) Representative blots of COX-2 and miR-26b-5p expression in HTR-8/SVneo cells transfected with miR-26b mimics with or without treatment with CoCl₂, showing that CoCl₂-induced increase in COX-2 expression could be blocked in cells transfected with miR-26b mimics. (B) The bar graphs show the relative COX-2 expression after normalized with β-actin expression in each sample. *P < 0.05: CoCl₂ alone vs control. **P < 0.01: miR-26b mimics vs control. ^##P < 0.01: miR-26b mimics + CoCl₂ vs CoCl₂ alone. Data are expressed as mean ± SE from five independent experiments. (C) Production of PGE₂ by HTR-8/SVneo cells in the experiment described in A, showing that increase of PGE₂ formation induced by CoCl₂ was significantly attenuated in the cells transfected with miR-26b mimics. *P < 0.05: CoCl₂ alone vs control. ^#P < 0.05: miR-26b mimics + CoCl₂ vs CoCl₂ alone. Data are expressed as mean ± SE from six independent experiments. (D) The bar graphs show the relative expression of PGIS after normalized with β-actin expression in each sample. ^#P < 0.05: miR-26b mimics or miR-26b mimics + CoCl₂ vs CoCl₂ alone. Data are expressed as mean ± SE from five independent experiments. (E) Production of PGI₂ by HTR-8/SVneo cells in the experiment described in A. PGI₂ formation is reduced in the cells cultured with CoCl₂, which was partially prevented when the cells transfected with miR-26b mimics. *P < 0.05: CoCl₂ alone vs control. Data are expressed as mean ± SE from three independent experiments.