Deficiency of heat shock transcription factor 1 suppresses heat stress-associated increase in slow soleus muscle mass of mice.
OBJECTIVE
Effects of heat shock transcription factor 1 (HSF1) deficiency on heat stress-associated increase in slow soleus muscle mass of mice were investigated.


METHODS
Both HSF1-null and wild-type mice were randomly assigned to control and heat-stressed groups. Mice in heat-stressed group were exposed to heat stress (41 °C for 60 min) in an incubator without anaesthesia.


RESULTS
Significant increase in wet and dry weights, and protein content of soleus muscle in wild-type mice was observed seven days after the application of the heat stress. However, heat stress had no impact on soleus muscle mass in HSF1-null mice. Neither type of mice exhibited much effect of heat stress on HSF mRNA expression (HSF1, HSF2 and HSF4). On the other hand, heat stress upregulated heat shock proteins (HSPs) at the mRNA (HSP72) and protein (HSP72 and HSP110) levels in wild-type mice, but not in HSF1-null mice. The population of Pax7-positive nuclei relative to total myonuclei of soleus muscle in wild-type mice was significantly increased by heat stress, but not in HSF1-null mice. Furthermore, the absence of HSF1 gene suppressed heat stress-associated phosphorylation of Akt and p70 S6 kinase (p-p70S6K) in soleus muscle.


CONCLUSIONS
Heat stress-associated increase in skeletal muscle mass may be induced by HSF1 and/or HSF1-mediated stress response that activates muscle satellite cells and Akt/p70S6K signalling pathway.
Laboratory of Physiology, School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.
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Y
Ohno
Department of Physiology, Graduate School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.|Research Fellow of the Japan Society for the Promotion of Science, Tokyo, Japan.
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T
Egawa
Laboratory of Physiology, School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.
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Yokoyama
Department of Molecular Biology, Graduate School of Medicine, Yamaguchi University, Ube, Japan.
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Nakai
Faculty of Education, Yamaguchi University, Yamaguchi, Japan.
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Sugiura
Graduate School of Health and Sports Science, Doshisha University, Kyotanabe, Japan.
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Ohira
Hirosaki Gakuin University, Hirosaki, Japan.
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Yoshioka
Laboratory of Physiology, School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.|Department of Physiology, Graduate School of Health Sciences, Toyohashi SOZO University, Toyohashi, Japan.
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K
Goto
D000818:Animals; D004268:DNA-Binding Proteins / Q000172:deficiency*; D000076249:Heat Shock Transcription Factors; D018882:Heat Stress Disorders / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006358:Hot Temperature; D051379:Mice; D008819:Mice, Nude; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology*; D013312:Stress, Physiological / Q000502:physiology*; D014157:Transcription Factors / Q000172:deficiency*
D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins; C490017:Hsf1 protein, mouse; D014157:Transcription Factors
heat shock proteins; heat shock transcription factor 1; heat stress; satellite cell; skeletal muscle