Skip to main content
. 2019 May 9;10:485. doi: 10.3389/fphar.2019.00485

FIGURE 1.

FIGURE 1

ATRA inhibited neointimal hyperplasia and suppressed the proliferation and migration of VSMC. (A) Representative sections of the left common carotid arteries from the sham group, ligation group and ATRA-treated groups by hematoxylin–eosin staining. (B) Morphometric quantification of intimal/media (I/M) ratio (n = 8). (C) A7r5 cells were incubated with the indicated doses of ATRA (1, 2 as well as 4 μM) for 24 h, followed by the MTS assay to determine the proliferation of A7r5 (n = 6). (D) A7r5 cells were treated with ATRA (4 μM) for 0, 24, 48, 72, 96, and 120 h, and MTS assay was performed to test cell proliferation rate (n = 6). (E) Representative images of EdU staining. EdU (in red) stained the regions of cell proliferation; Hoechst33342 (in blue) stained the nuclei. (F) Percentage of EdU positive cells of A7r5 (n = 3). (G) The expressions of CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 were tested via western blotting. (H) Relative levels of CyclinD1, CyclinD3, and CyclinA2 (n = 3). (I) Relative expression levels of CDK2, CDK4, and CDK6 (n = 3). (J) A7r5 cells were treated with different concentrations of ATRA (1, 2, and 4 μM), and tested by performing Transwell assays for 12 h. (K) The number of cells in each field of view (n = 5). Data are presented as mean ± SD. #p < 0.05, ##p < 0.01 compared with the ligation group. ∗p < 0.05, ∗∗p < 0.01 compared with the Control group.