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. 2020 Aug 27;40(10):2408–2424. doi: 10.1161/ATVBAHA.120.314333

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© 2020 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 4. — miR-217 expression promotes left ventricular dysfunction. A, Left ventricular diastolic function assessed as the ratio of Doppler-detected peak early diastolic velocity (E′) to peak late diastolic velocity (A′) in control apoE^−/− mice (miR-217^+/+ VE-Cad CreERT2^TG/+ apoE^−/−) and miR-217^KI apoE^−/− mice (miR-217^KI/+ VE-Cad CreERT2^TG/+ apoE^−/−) fed an HFD for 8 wk. Right, Representative echocardiography images. B, D2 pulmonary vein velocity in control apoE^−/− and miR-217^KI apoE^−/− mice fed an HFD for 8 wk. C, Left ventricular ejection fraction in control apoE^−/− and miR-217^KI apoE^−/− mice determined by echocardiography after 10 wk on an HFD. Data are from 2 independent experiments. Each dot represents an individual mouse. *P<0.05, **P<0.01 by unpaired t test (A–C). apoE indicates apolipoprotein E; LVID;d, left ventricular internal diameter in diastole; and LVID;s, left ventricular internal diameter in systole.