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. Author manuscript; available in PMC: 2020 Apr 16.
Published in final edited form as: Circulation. 2019 Apr 16;139(16):1913–1936. doi: 10.1161/CIRCULATIONAHA.118.033552

Figure 4. Cardiac-specific Fundc1 knockout (KO) inhibits diabetes-induced MAM formation.

Figure 4.

A, Western blot analysis of the interest proteins in cardiac homogenates prepared from vehicle- or STZ-treated WT or cardiac Fundc1 KO mice at the age of 6 months. Densitometric analysis of the blots is shown in the lower panel (mean ± SD, n = 8 mice per group; *P < 0.05 versus WT & vehicle; †P < 0.05 versus WT & STZ). B, Genotyping results illustrating cardiac-specific Fundc1 deletion in Akita mice. C, Western blot analysis of the interest proteins in cardiac homogenates from WT, Fundc1 KO, Akita, and Fundc1 KO Akita mice at the age of 6 months. Densitometric analysis of the blots is shown in the right panel (mean ± SD, n = 8 mice per group; *P < 0.05 versus WT; † P < 0.05 versus Akita). D, Representative TEM images of ER and mitochondrial morphology in the cardiac muscle of WT, Fundc1 KO, Akita, and Fundc1 KO Akita mice at the age of 6 months. The red stars indicate mitochondria, and the blue asterisks indicate ER. E, Quantitation of ER length adjacent to mitochondria, normalized to total ER length (mean ± SD, n = 5~7 mice per group; *P < 0.05 versus WT; † P < 0.05 versus Akita).