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Two previous studies have validated the immunomorphologic approaches presented herein by documenting good agreement between biochemical and immunomorphologic analyses in an experimental model of oxidative stress (iron nitrilotriacetate-induced injury of rat kidney [14] and analysis of oxidative damage in skeletal muscle of aging rhesus monkey [15]).
How are miR-29 levels increased in muscle of aging rodents?
This study provides a comprehensive analysis of genome-wide DNA methylation patterns in the skeletal muscle of aging pigs.
In summary, the present study provides a comprehensive analysis of genome-wide DNA methylation patterns in the skeletal muscle of aging pigs.
These results, together with our data, indicate that a decrease of miR-124 can be considered as a common signature in the liver and muscle of aging mice.
This would suggest there should be a lower level of miR-29 in muscle and possibly other tissues [ 51] but we and others have found that miR-29 is consistently up-regulated at least in muscle of aging rodents.
Similar(53)
Impaired signal transduction pathways have also been described in smooth muscle of ageing rat colon (Bitar 2003; Somara et al. 2007; Saffrey 2014).
In all species, tissues (including skeletal muscle) of aged organisms contain oxidative damage to lipids, DNA, and proteins compared with that found in young organisms (11, 50, 55); also, the hypothesis that increased oxidative damage plays a key role in age-related tissue dysfunction has been extensively examined.
In addition, we find that miR-29 is maintained at a high level in muscles of aging rodents.
In line with this, heat shock proteins, DNA repair genes and oxidative stress resistance pathways are activated in the muscles of aging mice (Park and Prolla, 2005).
Decreased NAD levels and NAD/NADH redox ratio were also observed in skeletal muscles of aging mice and monkeys, respectively (Gomes et al. 2013; Pugh et al. 2013).
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