Fig. 5: Desmin deficiency in iCMs leads to major delays in myofibrillogenesis and defects in Ca2+ influx. | Cell Death & Disease

Fig. 5: Desmin deficiency in iCMs leads to major delays in myofibrillogenesis and defects in Ca2+ influx.

From: Molecular insights into the role of desmin intermediate filament network in chromatin landscape, cardiomyocyte differentiation, and maturation

Fig. 5

A, B Confocal microscopy images of (A) mitotracker red (red) and α-actinin (green) on i) iCMsDes+/+ and ii) iCMsDes−/−, 5 weeks after GMT transduction: red arrows show co-alignment of mitotracker with α-actinin. There is a better alignment of the mitochondrial network with Z-lines in the presence of desmin. B Mitochondrial staining with the mitochondrial matrix protein SDHA (red) on iCMsDes+/+ and iCMsDes−/−, 5 weeks after GMT transduction, shows a diffused and fragmented mitochondrial network when desmin is absent. DAPI: blue staining of nuclei. Scale bars: 25 μm. C Representative electron microscopy images of i) neonatal cardiomyocytes of Des+/+ (NCMDes+/+), ii) iCMDes+/+ and iii) iCMDes−/−: red arrows point to z-discs of assembled myofibrils, obvious in iCMDes+/+ and absent in iCMDes−/−. While more than 90% of the iCMDes+/+ cultures show myofibril formation, less than 10% of the iCMDes−/− ones show any. Scale bars: 500 nm. D Representative calcium transient traces from the indicated cell types depicted as Fura-2-AM ratios (340/380 nm).

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