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. Author manuscript; available in PMC: 2012 Sep 13.
Published in final edited form as: Dev Cell. 2011 Sep 13;21(3):469–478. doi: 10.1016/j.devcel.2011.08.008

Figure 3. Mitochondrial structure and function changes after closure of the mPTP.

Figure 3

(A) Epifluorescence microscopy of MTG in live E9.5 cultured ventricular myocytes: WT, WT with 500 nM Cyclosporin A (CsA) for 2 hours, and CyP-D null (CyP-D KO) myocytes. (B) Mitochondrial length in cultured WT E9.5 myocytes with and without treatment with 500 nM CsA or 500 nM FK-506 for 2 hours, CyP-D null E9.5 myocytes, and WT E11.5 and 13.5 myocytes (*P<0.05 compared to WT E9.5). (C) Electron micrographs of WT E9.5 and CyP-D null E9.5 hearts. (D) A histogram of mitochondrial ultrastructure classes in electron micrographs from ventricular myocytes of WT E9.5, 11.5, 13.5, or CyP-D null E9.5 hearts. (E) Images of E9.5 cultured ventricular myocytes stained with calcein-AM in the presence of CoCl2. Quantification showed increased calcein fluorescence after treatment with 500 nM CsA (*P<0.05). (F and G) Measurements of Δψm (F) and ROS (G) in cultured WT E9.5 myocytes with and without treatment with 500 nM CsA or 500 nM FK-506 for 2 hours, CyP-D null E9.5 myocytes, and WT E11.5 and 13.5 myocytes (*P<0.05 compared to WT E9.5). Expanded graphical data is provided in Figure S2C–E.