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Muscle specificity of age‐related changes in markers of autophagy (863.9)
Author(s) -
Russ David,
McCoy Katherine,
Boyd Iva
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.863.9
Subject(s) - autophagy , sarcopenia , soleus muscle , skeletal muscle , medicine , endocrinology , ageing , parkin , senescence , chemistry , biology , biochemistry , apoptosis , disease , parkinson's disease
The purpose of this investigation was to determine the degree, if any, of muscle‐specificity regarding the effect of aging on markers of autophagy in skeletal muscle. The idea that impaired basal autophagy may contribute to age‐related declines in tissue and organ function has gained traction in recent years. Our own laboratory has reported that aging phasic hindlimb muscles of aging rats exhibit some signs of impaired autophagy, along with marked declines in force generating capacity, even in the absence of sarcopenia. However, age‐related declines appear to occur to a lesser degree, or lesser rate, in the tonic soleus muscle. Accordingly, here we examined expression, via immunblotting, of several markers of autophagy and stress in the medial gastrocnemius (MG) and soleus (SOL) muscles of adult (6‐8 months) and aged (24‐25 months) male, F344/BN rats (n = 7/grp). Two‐way ANOVA (age X muscle) revealed significant age X muscle interactions in several markers of autophagic signaling and ER stress (Atg3, Beclin, Parkin, Grp78),but not others (Atg7, Atg4b). Where interactions were present, age increased expression in the MG (+25‐50%), but not the soleus. Interestingly, the LC3b‐II/I ratio, a common index of autophagy was reduced in the MG, but not the soleus. This change difference was largely driven by age‐related increases in LC3b‐I, without increases in LC3b‐II. These data are consistent with age‐related failure of autophagic (perhaps at Atg7 or Atg4b) contributing to functional decline in the MG, but not the soleus. These data have important implications for mechanisms of muscular senescence and may direct the development of future intervention strategies to enhance aging muscle function.