Figure 5 | Scientific Reports

Figure 5

From: Endothelial-derived extracellular microRNA-92a promotes arterial stiffness by regulating phenotype changes of vascular smooth muscle cells

Figure 5

LNA-miR-92a reduces hypertension susceptibility. (A) Experimental design of mouse study. Ang II was released by osmotic minipumps at 1 μg/kg/min for 4 weeks. One week before Ang II infusion, LNA-control (LNA-Ctrl) or LNA-miR-92a was delivered at 16 mg/kg body weight via tail-vein injection, followed by a second dose of LNA-Ctrl or LNA-miR-92a delivery 10 days after the Ang II minipump implantation. The animals were sacrificed at the end of 4-week post-minipump implantation. (B) miR-92a level was measured in CD144+-EVs isolated from serum (n = 8). (C) Left carotid artery PWV (n = 8). (D) Correlation between the level of serum miR-92a and PWV. (E, F) Ambulatory SBP and DBP (n = 8). (G, H) Thoracic aortic rings were isolated from three groups of mice (n = 5). Representative traces of the ACh- (G) and SNP-induced (H) relaxation of Phe-precontracted rings. The dots represented cumulative addition of increasing doses of ACh and SNP (5 × 10–10 to 10–4 M). (I) qPCR analysis of miR-92a level in aortic ECs and SMCs from mice (n = 6). (J) qPCR analysis of indicated genes in aortas from mice (n = 8). Data are mean ± SEM. Normally distributed data were analyzed by the one-way ANOVA (B, C, ECs in I, smtn, calponin, FN, OPN and Thbs in J) between multiple groups. Normally distributed data (E–H) were analyzed by the two-way ANOVA between multiple groups. Non-normally distributed data were analyzed by the Kruskal–Wallis test (SMCs in I, α-SMA in J) between multiple groups. *p < 0.05 vs. Saline, #p < 0.05 vs. Ang II + LNA-Ctrl. *p < 0.05, **p < 0.01, ***p < 0.001. rs, Spearman correlation coefficient.

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