Key result
Rearrangement of the contractile apparatus in cultured cardiomyocytes is accompanied by the release of key structural sarcomeric proteins from actin structures into the cytoplasm as inclusions.
The study demonstrates that smooth muscle actin is incompatible with sarcomeric isoforms of key structural proteins and myofibrillar organization in cultured cardiomyocytes.
Does not alter clinical management; leaves open in vivo relevance of sarcomeric protein dynamics.
Cardiomyocytes in culture undergo reversible rearrangement of their contractile apparatus with conversion of typical myofibrils into structures resembling stress fibers of nonmuscle cells. Such rearrangement is accompanied by the replacement of cardiac actin, the main protein of myofibrils, with its smooth muscle isoform. This study shows that along with the replacement of actin isoform the key structural sarcomeric proteins are released from actin structures and stored in cell cytoplasm as inclusions not bound with actin. The data obtained are indicative of the incompatibility of smooth muscle actin with sarcomeric isoforms of these proteins and myofibrillar organization in general.
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Bildyug et al. (2019) studied Cardiomyocytes in culture. Rearrangement of contractile apparatus was evaluated on Redistribution of sarcomeric myosin and α-actinin. Rearrangement of the contractile apparatus in cultured cardiomyocytes is accompanied by the release of key structural sarcomeric proteins from actin structures into the cytoplasm as inclusions.
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