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. 2016 Feb 3;7:10521. doi: 10.1038/ncomms10521

Figure 8. Inhibition of the interaction between miR-103 and KLF4 limits atherosclerosis.

Figure 8

(a) Immunostaining of KLF4 and von Willebrand factor (vWF) in aortic root sections of Apoe−/− mice treated with KLF4-TSBs or non-targeting LNA-oligonucleotides (control). Representative images are shown. Atherosclerosis (b) quantified in Oil red O-stained, en face prepared aortas and the lesional macrophage cell number (c) determined by MAC2 immunostaining in aortic root lesions from Apoe−/− mice treated with KLF4-TSBs or control oligonucleotides (n=4–6 mice per group). (d) Dual immunostaining of CXCL1 and vWF in aortic root sections of Apoe−/− mice treated with KLF4-TSBs or control oligonucleotides. (e) The expression levels of Cxcl1 in the carotid, liver, spleen and heart of KLF4-TSB-treated Apoe−/− mice compared with control mice (n=4–7 mice per group). (f) Dual immunostaining of eNOS and vWF in aortic root sections of Apoe−/− mice treated with KLF4-TSBs or control oligonucleotides. (g) Nos3 mRNA expression in the carotid arteries of KLF4-TSB-treated Apoe−/− mice compared with control mice (n=5–6 mice per group). The nuclei were counterstained with 4',6-diamidino-2-phenylindole (DAPI). Asterisks indicate the lumen. Representative images of three independent experiments are shown. Scale bars, 10 μm (f), 25 μm (a,d), 50 μm (c) and 1 mm (b). The data are represented as the mean±s.e.m. of the indicated number (n) of repeats. *P<0.05 and **P<0.01 by Student's t-test.