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. 2024 May 21;121(22):e2402890121. doi: 10.1073/pnas.2402890121

Fig. 2.

Fig. 2.

Lack of core M glycans on α-DG in cardiac muscle leads to progressive cardiomyopathy. (A) Alpha-DG core M modification in control and Pomt1 cKO. (B–D) Immunoblots on ventricles to detect B, matriglycan; C, core α-DG/β-DG; and D, laminin binding. Two sets of pooled samples per group (control n = 13; cKO n = 11). (E) Immunofluorescence on ventricles to detect matriglycan and β-DG (n = 12 controls; n = 12 cKO mice). (Scale bar, 100 μm.) (F) Immunofluorescence on ventricles from 120-wk-old mice to detect fibrotic accumulation. (Scale bar, 1 mm.) (G) Heart weight per tibial length (HW/TL); (H) left ventricular end diastolic volume per left ventricular mass (LV EDV/Mass); and (I) LV ejection fraction in 30-, 60-, and 90-120-wk-old mice. Mice of both sexes were utilized. Number of mice for HW/TL and echocardiography: controls = 5; cKO = 4 at 30-wk; controls = 4, cKO = 5 at 60-wk; controls = 3, cKO = 5 for HW/TL at 90 to 120-wk; and controls = 3, cKO = 3 for echocardiography at 90 to 120-wk. *P < 0.05. Unpaired t tests with the Holm–Sidak post hoc test performed on age-matched groups. Data expressed as mean ± SD.