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. Author manuscript; available in PMC: 2022 Sep 14.
Published in final edited form as: Immunity. 2021 Jul 27;54(9):2072–2088.e7. doi: 10.1016/j.immuni.2021.07.003

Figure 2. CCR2− macrophages influence survival and LV remodeling in dilated cardiomyopathy.

Figure 2.

A, Schematic of experimental groups, CCR2− macrophage depletion strategy, and endpoints. B, CD68 immunostaining of control, CD169-DTR, Tnnt2ΔK210/ΔK210, and Tnnt2ΔK210/ΔK210 CD169-DTR hearts after 3 weeks of DT treatment. n=4 per group. Scale bar: 20μm. C, Quantification of CD68 immunostaining. ** denotes p<0.05 (ANOVA, Post-hoc Tukey) compared to all other groups. D, Flow cytometry of CD45+Ly6G−CD64+ macrophages showing specific depletion of CCR2− macrophages in Tnnt2ΔK210/ΔK210 CD169-DTR hearts. n=4 per group. E, Kaplan-Meier analysis of survival in control, CD169-DTR, Tnnt2ΔK210/ΔK210, and Tnnt2ΔK210/ΔK210 CD169-DTR mice after DT treatment. n=12–15 per group. F-I, LV ejection fraction, relative wall thickness, LV volumes (μl), and stroke volume in control, CD169-DTR, Tnnt2ΔK210/ΔK210, and Tnnt2ΔK210/ΔK210 CD169-DTR mice 3 weeks after DT treatment. n=4–8 per group. * denotes p<0.05 (ANOVA, Post-hoc Tukey) compared to controls. # denotes p<0.05 compared to Tnnt2ΔK210/ΔK210 mice. J, Pressure volume loops showing reduced stroke volume in Tnnt2ΔK210/ΔK210 CD169-DTR compared to Tnnt2ΔK210/ΔK210 mice. n=4 per group. K, Invasive hemodynamics: LV dP/dt max, heart rate (HR), and LV end systolic pressure (LVESP) at baseline and during peak infusion of dobutamine (64 ng/min) in control, CD169-DTR, Tnnt2ΔK210/ΔK210, and Tnnt20394K210/ΔK210 CD169-DTR mice 3 weeks after DT treatment. n=5 per group. * denotes p<0.05 (ANOVA, Post-hoc Tukey) compared to controls. # denotes p<0.05 compared to Tnnt2ΔK210/ΔK210 mice. See also Figure S4–6, Tables S2–S3.