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. 2011 May;8(5):711–718. doi: 10.1016/j.hrthm.2011.01.010

Figure 3.

Figure 3

Molecular changes in desmosomal and gap junction proteins in the patient's myocardium. A: Western blot analysis in the patient (P) compared to nonfailing control tissue (NF). Samples were assayed for desmosomal proteins and connexin43 (Cx43). Blotting for desmin (DES), sarcomeric markers alpha-actinin (ACTN), and myosin heavy chain (MyHC) served as loading controls. B: High-resolution Western blotting of Cx43 identified two different bands in the control sample (arrows 1 and 2), whereas the dominating band in the patient sample migrated even faster (arrow 3) The position of marker proteins (molecular weight in kilodaltons) is indicated. C: Reduced total Cx43 protein levels in the patient sample (Cx43 normalized to desmin, NF set to 1, N = 3). D: Confocal immunofluorescence microscopy analysis for Cx43 in control and patient myocardial sample showed normal localization of Cx43 at the intercalated disks. Scale bar at lower left in each panel represents 10 μm. DSC2 = desmocollin-2; DSG2 = desmoglein-2; DSP = desmoplakin; PG = plakoglobin; PKP2 = plakophilin-2.