Fig. 4: T1-EXO and miR-222 promoted HA-VSMCs proliferation. | Cell Death & Disease

Fig. 4: T1-EXO and miR-222 promoted HA-VSMCs proliferation.

From: Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway

Fig. 4

a–c The effect of different concentrations of T1-EXO on HA-VSMCs proliferation was detected by CCK8. *P < 0.05, versus control group; †P < 0.05, versus 1.5 μg/mL group; ‡P < 0.05, versus 3 μg/mL group. n = 5, each group. d–f The pro-proliferative effect of optimal concentration of T1-EXO and mir-222-up lentivirus in HA-VSMCs was compared by CCK8. *P < 0.05, versus control group. n = 5, each group. g–j Representative EdU-stained VSMC photomicrographs from different groups. Note: green color is EdU positive cell; blue color is nucleus stained by Hoechst 33342. *P < 0.05, versus control group. n = 3, each group. k, l T1-EXO and miR-222 modulates HA-VSMC proliferation by regulating proteins that control cell cycle. T1-EXO and miR-222 down-regulated the expression of CDKN1B and CDKN1C but upregulated the expression of Cyclin D1 in HA-VSMC. β-actin expressions served as internal control. The control group was set to 1. *P < 0.05, versus control group. n = 3, each group. All data were expressed as mean ± SEM from three individual experiments

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