Words similar to hypertrophic
Example sentences for: hypertrophic
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Combined with the fact that some, albeit fewer, hypertrophic cells are present, the accumulation of proliferating chondrocytes suggests that Hoxc-8 regulates the rate of progression of chondrocytes to maturity [ 1 ] . In line with this interpretation, the in vivo BrdU incorporation assays suggested that cell cycle progression of chondrocytes may be decreased in transgenic animals with higher Hoxc-8 transgene expression levels.
A loop present in the motor domain called the HCM (mutations in this loop cause hypertrophic cardiomyopathy) is the location of a phosphorylatable serine (S) or threonine (T) in certain amoeboid myosin I molecules and myosin VI molecules.
This would be expected chronically to result in a eccentric hypertrophic pattern, a condition that we and others [ 15 17 ] have found in iron deficient rat hearts.
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 ] .
Many studies have shown that chronic intravenous infusion of norepinephrine is sufficient to cause hypertrophy, and that various forms of hypertrophy are linked to a decrease in either beta-adrenergic receptor density or a decreased responsiveness to beta-adrenergic stimulation [ 46 48 49 56 57 58 59 60 61 62 63 ] . Barth, for example, showed that norepinephrine infusion induced left ventricular hypertrophy that could be prevented by an adrenergic-receptor blocker [ 58 ] . It has been suggested that ornithine decarboxylase is a link between beta-adrenoreceptors and stimulation of tissue growth factor, which results in hypertrophy [ 64 ] . However, recent studies have focused on alpha-adrenergic reception as a mediator of cardiac hypertrophy [ 35 ] , although some question the role of the alpha-adrenergic receptor as a hypertrophic mediator in vivo [ 34 ] . To date, no published studies of which we are aware have examined alpha-adrenergic reception and the development of cardiac hypertrophy with iron deficiency.
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