FIGURE 5.

miR-9 relieves atherosclerosis by disrupting the SDC2-dependent FAK/ERK signaling pathway in mice. (A) miR-9 expression patterns determined by RT-qPCR in the aortic lysate of mice treated with miR-9 agomir, normalized to U6; (B) SDC2 mRNA expression patterns determined by RT-qPCR in the aortic lysate of mice treated with miR-9 agomir or in combination with oe-SDC2, normalized to GAPDH; (C) Representative Western blots of SDC2 protein and its quantitation in the aortic lysate of mice treated with miR-9 agomir or in combination with oe-SDC2, normalized to GAPDH; (D) Representative Western blots of FAK, and ERK1/2 proteins and their quantitation in the aortic lysate of mice treated with miR-9 agomir or in combination with oe-SDC2, normalized to GAPDH; (E) Aortic plaque area measured using oil red O staining in mice treated with miR-9 agomir or in combination with oe-SDC2; (F) The lesion degree of aorta determined using HE staining in mice treated with miR-9 agomir or in combination with oe-SDC2 (400×); (G) The proliferation of collagen fibers determined using Masson’s trichrome staining in aorta of mice treated with miR-9 agomir or in combination with oe-SDC2 (200×); and (H) Mac-3-labeled macrophages surrounding the aorta were measured using immunohistochemistry in mice treated with miR-9 agomir or in combination with oe-SDC2 (400×); *p < 0.05 vs. mice treated with agomir NC; n = 8 for mice upon each treatment. All data were measurement data and expressed as mean ± standard deviation. Comparisons were analyzed using the unpaired t-test. The experiment was repeated 3 times.