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CAVEOLIN-3
IS UP-REGULATED IN THE PHYSIOLOGICAL LEFT VENTRICULAR HYPERTROPHY INDUCED
BY VOLUNTARY EXERCISE TRAINING IN RATS
Teruhiko Aoyagi1 ,
Yoshihiro Ishikawa2, Hitosh Oshikawa2, Koichiro
Kinugawa3, Ikuo Yokoyama3 and Ryozo Nagai3
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1 Department
of Cardiovascular Medicine, Japanese Red Cross Medical Center, Tokyo,
Japan.
2 Department of Physiology, Yokohama City University, School
of Medicine, Yokohama, Japan.
3 Department of Cardiovascular Medicine, University of Tokyo,
Tokyo, Japan.
| Received |
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16 September 2002 |
| Accepted |
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12
November 2002 |
| Published |
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01 December 2002 |
© Journal of Sports Science
and Medicine (2002) 1, 141 - 146
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Various
substances have been introduced in relation with cardiac hypertrophy almost
always with controversy in their roles in signal transduction. Those controversies
may attribute to the diversity of cardiac hypertrophy. We previously showed
that calcineurin was activated in physiological left ventricular hypertrophy
(LVH) induced by voluntary exercise training, but not in decompensated pressure-overload
LVH. In the current study, we advanced our search for the differences between
the voluntary exercise-induced LVH and the pressure-overload LVH into several
other hypertrophy-related substances including caveolin. Wistar rats were
assigned to one of the following three groups: 10 weeks of voluntary exercise
(EX), sedentary regimen (SED), and 4 weeks of ascending aortic constriction
(AC). The EX rats voluntarily ran 1.6±1.1 km/day in the specially manufactured
cages resulting in LVH (24 % increase in left ventricular weight per body
weight ratio). Myocardial tissue homogenate of the EX rats revealed different
characteristics in signal transduction of hypertrophy from that of the AC.
The EX rats had normal sarcoplasmic reticulum (SR) Ca2+ATPase
mRNA level and normal myosin heavy chain isozyme pattern assessed by RNA
protection assay, while AC rats had decreased SR Ca2+ATPase mRNA
level and increased beta myosin heavy chain mRNA level. Myocardial caveolin-3
protein levels assessed by Western blotting increased in the EX rats but
decreased in the AC rats. The voluntary exercise-induced LVH differed in
signal transduction from the decompensated pressure-overload LVH. Caveolin-3
was induced in the voluntary exercise-induced LVH, while it was decreased
in the decompensated pressure-overload LVH.
KEY WORDS: Exercise, hypertrophy, signal transduction.
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