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

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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.