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. Author manuscript; available in PMC: 2016 Jul 7.
Published in final edited form as: Cell Rep. 2015 Jun 25;12(1):15–22. doi: 10.1016/j.celrep.2015.06.002

Figure 2. Loss of MCU from the adult heart does not lead to pathology at baseline or with pathologic stress stimulation.

Figure 2

(A) Time-course for the analyses of cardiac function in response to aging following Mcu deletion.

(B) Transverse H&E heart sections at 200X magnification.

(C) Representative electron micrographs from heart sections. Scale bar is 500 nm.

(D and F) Heart-weight normalized to body-weight ratios (HW/BW) at 18 and 52 weeks of age.

(E and G) Echocardiographic measurement of fractional shortening (FS%) at 18 and 52 weeks of age.

(H) Time course for generation of mice and analyses of cardiac function following TAC surgery.

(I) H&E-stained transverse heart sections 8 weeks after TAC surgery, at 200X magnification.

(J-L) HW/BW, (K) cardiomyocyte cross-sectional area and (L) FS% in the indicated groups of mice 8 weeks following TAC.

All values reported as mean ± SEM. *P<0.05 versus Mcufl/fl sham

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