Words similar to myocyte
Example sentences for: myocyte
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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.
have demonstrated that spontaneously hypertensive rats(SHR) with symptoms of heart failure had significantly higher levels ofapoptotic myocytes than control myocytes [ 37 ] .When treated with an angiotensin-converting enzyme inhibitor, thenumber of apoptotic cells in the SHR with symptoms of heart failurewas dramatically reduced to control levels; controls were SHR withoutsymptoms of heart failure [ 37 ] . Kajstura et al.have also reported that angiotensin II increased the percentageof apoptotic cells in isolated adult rat ventricular myocytes, andthis effect was mediated by AT-1 receptors [ 38 ] .Although ventricular function was not assessed in these studies,the observations raise the possibility that, like our findings withcarvedilol, the beneficial effect of ACE-inhibitors or AT-1 receptorblockers in heart failure may in part be attributed to an inhibitionof myocyte apoptosis with a resultant improvement in in vivo cardiacfunction, a concept that needs further study.
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.
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 ] .
This observation represents animportant finding in demonstrating the effectiveness of a cardiovasculardrug to protect against continual cardiac myocyte apoptosis in failinghearts in vivo . Furthermore, the inhibition of apoptosisby carvedilol was accompanied by signs of improvement in left ventricularfunction and heart size (i.e.
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