The effects of Xin shRNA with cardiotoxin injury on skeletal muscle in vivo

Xin, an actin binding protein, has been implicated in the regulation of satellite cells during skeletal muscle regeneration. It is believed to exert effects on the cytoskeleton through interactions with other structural proteins like filamin c, f‐actin and desmin. In order to investigate the role of Xin in muscle regeneration following injury, we injected Xin shRNA adenovirus (XinAd) into the right tibialis anterior (R‐TA) of male C57B6 mice while the left tibialis anterior (L‐TA) served as a control. Muscle injury in both legs was induced 4 days later using a cardiotoxin injection. As expected, XinAd reduced endogenous Xin expression by 67.8 ± 7.4% at 0 days. Surprisingly, at 3 days Xin Ad injected muscle displayed 29.3 ± 8.1% increase in filamin c, 12.6 ± 5.6% increase in f‐actin and a 41.2 ± 12.9% decrease in desmin expression compared to the L‐TA. Histochemically, the treatment and control tissues illustrated similar signs of degradation and regeneration at all time points. Therefore, while silencing Xin modifies actin‐associated protein expression patterns, it appears that other factors may compensate for its disappearance in terms of whole muscle regeneration.