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Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, Fukuoka 812-82; and Department of Pathology, Mie University, Tsu 514, Japan
Mechanical
overloading to cardiac muscle causes fetal contractile protein gene
expression and acceleration of protein synthesis. Myocyte microtubules
might be involved in these pressure overload-induced hypertrophic
responses. We assessed c-fos and fetal
contractile protein genes such as 
-myosin heavy chain (MHC) and
-skeletal actin using Northern blot analysis and quantified total
cardiac protein, DNA, and RNA content in the left ventricular
myocardium obtained from four groups of rats: sham-operated rats;
sham-operated rats treated with colchicine, which depolymerized
microtubules; rats in which acute pressure overload was imposed by
abdominal aortic constriction for 3 days (AoC); and AoC rats treated
with colchicine (AoC + colchicine). Systolic arterial pressure was elevated to a similar degree in AoC and AoC + colchicine rats. c-fos and -MHC mRNA levels were
significantly upregulated in AoC rats, which was attenuated by
microtubule inhibition. Both RNA content and RNA-to-DNA ratio, the
index of the protein synthesis capacity, were increased in AoC rats,
which effect was also abolished by colchicine. Furthermore, induction
of nonfunctioning microtubules by taxol or deuterium oxide exerted the
same inhibitory effects. Thus the hypertrophic responses of the
myocardium during pressure overload might depend on the integrity of
myocyte microtubules.
protein; ribonucleic acid; cytoskeleton; myocyte
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