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. 2020 Dec 10;143(8):821–836. doi: 10.1161/CIRCULATIONAHA.120.044581

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© 2020 The Authors.

Circulation 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 License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 4. — Blockade of DC cross-priming protects mice from adverse remodeling and functional decline after ischemic injury. C57BL/6J (WT) and Clec9a^−/− C57BL/6J (KO) mice were treated with 160 mg/kg isoproterenol to induce T2MI-like injury and heart function was assessed by electrocardiography, optical mapping and transthoracic echocardiography. A, Heart rate of isoproterenol-treated WT and KO mice 2 weeks after challenge. B, Schematic showing features of electrocardiography traces. C, Quantification of QRS duration in electrocardiography traces of isoproterenol-treated WT and KO mice 2 weeks after challenge and corresponding fold change of QRS duration in both strains. Symbols represent individual mice. D, Summary of parameters obtained by electrocardiography and optical mapping. E, Parasternal long- and short-axis echocardiography B-mode view (blue lines in long and short axes) showing levels of M-mode traces (base, mid, apex) and obtained measurements. F, LV global function in isoproterenol-treated WT and KO mice as assessed by % ejection fraction (left) and fold decrease from baseline (right). G, LV dilation in isoproterenol-treated WT and KO mice as assessed by LV end-systolic volume (left) and fold increase from baseline (right). H, Summary of echocardiography parameters obtained by echocardiography M-mode traces from both the parasternal long- and short-axis view; n=6/group. Error bars show mean±SEM; *P<0.05; **P<0.001; ***P<0.0001; 2-way ANOVA with Sidak multiple comparisons post hoc test (A, C, F, G); 2-tailed Student t test (C and D); repeat measures 2-way ANOVA with Sidak multiple comparisons post hoc test (F and G); 1-way ANOVA with Dunnett multiple comparisons post hoc test (H); multiplicity-adjusted P values. APD, action potential duration; ctrl, control; d, diastole; d0, day 0; dV/dt, rate of action potential rise; EDV, end diastolic volume; EF, ejection fraction; ESV; end systolic volume; FS, fractional shortening; ISO, isoproterenol; IVS, interventricular septum (thickness); KO, knockout; LV, left ventricular; LVID, left ventricular internal dimension; LVPW, left ventricular posterior wall (thickness); s, systole; w2, week 2; w4, week 4; and WT, wild type.