Postnatal changes in caldesmon expression and localization in cardiac myocytes

Abstract

Caldesmon is a heat-stable protein found in both muscle and non-muscle tissue. It binds to a number of contractile and cytoskeletal proteins and may be involved in regulating acto-myosin interaction in smooth muscle cells and/or the assembly of microfilaments in muscle and non-muscle cells. We have shown previously that caldesmon is localized at the Z-lines in adult cardiac myocytes and that both the low-and high-molecular-weight forms ( l -caldesmon and hcaldesmon, respectively) are present in atrial and ventricular myocytes. Here we examined the expression of caldesmon and its localization in freshly isolated cardiac myocytes during postnatal development and when these myocytes were grown in culture. We found that l -caldesmon is expressed in both neonatal and adult rat ventricular myocytes.The expression of h -caldesmon, however, was not detected in myocytes from newborn animals but increased during the first 2 weeks of postnatal development. Caldesmon was generally not co-localized with α -actinin at the Z-lines in neonatal myocytes but became increasingly more so during the first 2 weeks of postnatal development. When myocytes from 5-and 10-day-old rats were grown in primary culture, h -caldesmon expression decreased and caldesmon could not be detected at the Z-lines in the cultured cells. These results indicate that caldesmon plays a role at the Z-lines in adult cardiac myocytes; however, its localization at the Z-lines is not necessary for the prenatal development that occurs at these sites or for the establishment of a contractile phenotype in cultured cardiac myocytes.

Transcriptional and Functional Profiling of Human Embryonic Stem Cell-Derived Cardiomyocytes

“…There are also considerable reductions in the expression of a number of homeobox genes (HOXB3, 4, IRX, HHEX, HESX1). At the same time, we observe substantial increases in expression of 1,012 genes, including cardiac structural genes such as tropomyosin 1 and 2 (TPM1, 2, ∼3 fold upregulated) [15] , the heart and muscle gene LMO7 (3.5 fold) [16] , and a number of actins and actin-regulatory genes such as beta actin (ACTNB, 3.4 fold), alpha actinin (5 fold), coronin (2.5 fold), transgelin (4.6 fold) [17] , and caldesmon 1 (5 fold) [18] ( Table S1 (A4) ). Cells in this population also exhibit evidence of maturation with the increased expression of extracellular structural components such as vascular collagens COL8A1 (18 fold) [19] , COL4A3 and 4 (11 fold and 16 fold) [20] , COL6A3 (4 fold) [21] , and COL2A1 (2.4 fold) [22] .…”

Methyl donor deficiency in H9c2 cardiomyoblasts induces ER stress as an important part of the proteome response

“…These proteins have a crucial role in organizing membrane domains as linkers between transmembrane proteins and the underlying cytoskeleton (McMartin et al, 2003;Ben-Aissa et al, 2012). Multiple MD deficiency with increased production of Hcy, might thus perturb the integrity of the cardiac cell membrane.…”