Words similar to hypertrophic
Example sentences for: hypertrophic
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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 ] .
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.
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.
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.
Whether the elevated Ihh mRNA levels originate from increased expression in cells that make Ihh normally (prehypertrophic and hypertrophic chondrocytes) or from ectopic activation by the Hox transcription factors in proliferating cells, remains to be investigated.
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