Title:Increased Heat Shock Protein Expression Decreases Inflammation in Skeletal Muscle During and after Frostbite Injury
Volume: 20
Issue: 9
Author(s): Tomas Liskutin, Jason Batey, Ruojia Li, Colin Schweigert and Ruben Mestril*
Affiliation:
- Dept. Cell and Molecular Physiology, Loyola University Chicago, Health Sciences Division, Maywood, IL,United States
Keywords:
Frostbite injury, heat shock proteins, hsp90 inhibitor, 17-DMAG, skeletal muscle, inflammation.
Abstract:
Background: Frostbite injury results in serious skeletal muscle damage. The
inflammatory response due to frostbite causes local muscle degeneration. Previous
studies have shown that heat shock proteins (hsps) can protect against inflammation. In
addition, our previous studies showed that increased expression of hsp70 is able to
protect skeletal muscle against cryolesion.
Methods: Therefore, our aim was to determine if the induction of the heat shock
proteins are able to minimize inflammation and protect skeletal muscle against frostbite
injury.
Results: In the present study, we used the hsp90 inhibitor, 17-dimethylaminoethylamino-
17-demethoxygeldanamycin (17-DMAG), which was administered within 30
minutes following frostbite injury. Rat hind-limb muscles injected with 17-DMAG
following frostbite injury exhibited less inflammatory cell infiltration as compared to
control rat hind-limb muscles. In agreement with this observation, it has been observed
that increased hsp expression resulted in decreased inflammatory cytokine expression.
Additionally, we found that the administration of 17-DMAG after frostbite injury can
preserve muscle tissue structure as well as function.
Conclusion: It has been concluded that compounds such as 17-DMAG that induce the
heat shock proteins are able to preserve skeletal muscle function and structure if
injected within 30 minutes after frostbite injury. Our studies provide the basis for the
development of a potential therapeutic strategy to treat the injury caused by frostbite.
