Words similar to cardiomyocytes
Example sentences for: cardiomyocytes
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Previous studies have demonstrated the derivation of neural cells [1–3], hematopoietic [17] and endothelial lineages [18], and cardiomyocytes [19] from hESCs.
For two decades, the bulk of our knowledge of molecular pathways that guide cardiac growth, development, and disease has been gleaned from a combination of in vivo studies in genetically engineered mice and primary cultures of neonatal and adult rat cardiomyocytes.
Under defined in vitro conditions, these cells adopt a cardiomyocyte phenotype that goes beyond the simple expression of cardiac-restricted biochemical and molecular markers, extending to the types of single-cell physiological functions that are hallmarks of authentic cardiomyocytes, including action potentials, calcium transients, and contractile activity.
They call the cells Spoc cells, an acronym for “skeletal-based precursor of cardiomyocytes.”
is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .
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