Words similar to myocyte
Example sentences for: myocyte
How can you use “myocyte” in a sentence? Here are some example sentences to help you improve your vocabulary:
With the clear demonstration that cardiac myocyte apoptosis ispresent in our heart failure model strategies for prevention ofapoptosis can be tested.
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 ] .
The initial increase in circulating norepinephrineis thought to maintain cardiac function through inotropic mechanisms.However, a direct cardiac myocyte toxicity from norepinephrine iswell recognized [ 6 7 ] . Furthermore, pressure-overloadand stretch associated release of angiotensin II has been shownto induce myocyte apoptosis [ 8 9 10 ] .In an elegant paper by Telger et al.
The development of well-characterized cardiac progenitor cells offers the promise of using real genetic-based approaches to rapidly define the complex pathways that guide cardiac contractility, excitability, and lineage diversification into atrial, ventricular, and conduction system myocyte cell lineages.
Recent studies have proposed that myocyte loss incardiomyopathy can occur by apoptosis without an inflammatory response [reviewedin [ 1 2 3 ] ]. In heart failure,growth stimulation initially occurs as a compensatory effort tomeet chronically altered hemodynamic demands and is mediated by systemicand/or local up-regulation of mediators of adrenergic pathways andby various cytokines [ 4 5 ] . However, cytokinescan be directly toxic to cardiac myocytes and result in increasedapoptotic cell death [ 3 6 ] . Local up-regulationof angiotensin II induces immediate-early genes, which may leadto increased protein synthesis and myocardial hypertrophy or, alternatively,may up-regulate expression of apoptotic proteins (such as p53) incardiac myocytes.
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