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1 National Research Council
Unit for Muscle Biology and Physiopathology,
Congestive heart failure is characterized by a skeletal muscle
myopathy with muscle bulk loss. The mechanisms responsible for these
changes are not clear at present. We have investigated the role of
apoptosis in the rat "slow" soleus muscle during the development
of heart failure, which was induced by injection of monocrotaline (30 mg/kg). We looked at the time course of apoptosis by studying six
animals at each of the following time points: 0, 17, 24, and 30 days.
We found a decreased expression of the antiapoptotic protein Bcl-2,
which was accompanied by a rise of proapoptotic caspase-3. Ubiquitin
levels did not change. DNA nick-end labeling showed an increased number
of apoptotic nuclei both in myofibers and interstitial cells when heart
failure occurred. At variance with previous observations in the
fast-twitch tibialis anterior muscle in the same animals, in which
tumor necrosis factor-
(TNF-) increased at the time that
apoptosis occurred, the magnitude of apoptosis is lower in soleus
muscle and there is no appearance of muscle atrophy. In soleus muscle,
apoptosis is accompanied by activation of the caspase-3 system. There
is no activation of the TNF-- and ubiquitin-dependent protein waste.
In conclusion, slow muscles are less prone to develop apoptosis than
fast muscles. Muscle atrophy appears earlier in these latter ones.
Bcl-2; caspase-3
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