Research Paper Volume 11, Issue 22 pp 10016—10030

Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice

Figure 2. Atherosclerotic vulnerable plaque formation and intraplaque angiogenesis of ApoE knockout mice with AS are inhibited by H19 silencing. (A) The silencing efficiency of H19 assessed by RT-qPCR. * p < 0.05 vs. the NC-ASO group. (B) The atherosclerotic vulnerable plaque formation evaluated by HE staining (× 400) (The arrow referred to lipid vacuoles, * represented inflammatory cells and # indicated fractured smooth muscle.). (C) The number of new blood vessels measured by Immunohistochemical staining (× 400) (The arrow referred to CD34-positive cells). (D) The protein levels of MMP-2, VEGF, p53 and TIMP-1 in atherosclerotic plaques normalized to GAPDH after H19 silencing determined by Western blot analysis. * p < 0.05 vs. the NC-ASO group. The data were measurement data and expressed by mean ± standard deviation. Data differences between two groups were analyzed by unpaired t-test. n = 6. The experiment was repeated three times independently.