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Heat shock transcription factor 1‐associated expression of slow myosin heavy chain in mouse soleus muscle in response to unloading with or without reloading
Author(s) -
Yokoyama S.,
Ohno Y.,
Egawa T.,
Yasuhara K.,
Nakai A.,
Sugiura T.,
Ohira Y.,
Yoshioka T.,
Okita M.,
Origuchi T.,
Goto K.
Publication year - 2016
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12692
Subject(s) - nfat , myosin , population , transcription factor , microbiology and biotechnology , biology , chemistry , medicine , endocrinology , biochemistry , gene , environmental health
Aim The effects of heat shock transcription factor 1 ( HSF 1) deficiency on the fibre type composition and the expression level of nuclear factor of activated T cells ( NFAT ) family members ( NFAT c1, NFAT c2, NFAT c3 and NFAT c4), phosphorylated glycogen synthase kinase 3 α (p‐ GSK 3 α ) and p‐ GSK 3 β , micro RNA ‐208b (miR‐208b), miR‐499 and slow myosin heavy chain (My HC ) m RNA s (Myh7 and Myh7b) of antigravitational soleus muscle in response to unloading with or without reloading were investigated. Methods HSF 1‐null and wild‐type mice were subjected to continuous 2‐week hindlimb suspension followed by 2‐ or 4‐week ambulation recovery. Results In wild‐type mice, the relative population of slow type I fibres, the expression level of NFAT c2, p‐ GSK 3 ( α and β ), miR‐208b, miR‐499 and slow My HC m RNA s (Myh7 and Myh7b) were all decreased with hindlimb suspension, but recovered after it. Significant interactions between train and time (the relative population of slow type I fibres; P = 0.01, the expression level of NFAT c2; P = 0.001, p‐ GSK β ; P = 0.009, miR‐208b; P = 0.002, miR‐499; P = 0.04) suggested that these responses were suppressed in HSF 1‐null mice. Conclusion HSF 1 may be a molecule in the regulation of the expression of slow My HC as well as miR‐208b, miR‐499, NFAT c2 and p‐ GSK 3 ( α and β ) in mouse soleus muscle.