Background/Purpose: Myositis is a broad term for a group of rare autoimmune diseases that cause persistent muscle inflammation, weakness, and fatigue. Currently, first-line treatment for myositis includes glucocorticoids. However, this approach results in significant side effects and is ineffective in all patients. The receptor for advanced glycation endproducts (RAGE) plays an essential role in orchestrating cellular pathways leading to inflammatory processes. Furthermore, RAGE has been shown to be involved in multiple inflammatory conditions including diabetes, cancer, and DMD. This suggests that RAGE could be a promising target for treating autoimmune diseases, including myositis. Therefore, we investigated the expression of RAGE in a mouse model of myositis and myositis patient muscle.

Methods: Total RNA was isolated from skeletal muscle using the TRIzol® method and .5 µg used for cDNA synthesis. TaqMAN qPCR was performed and GAPDH was used as an internal control to normalize for gene expression. Expression levels of AGER and MOK were calculated relative to healthy controls using the 2-ΔΔ-Ct method. These target genes were chosen because they are involved in the production of the RAGE receptor.

Results: In myositis mice, both AGER and MOK expression were significantly increased compared to healthy control mice (p< 0.01 and p< 0.05, respectively).  Similarly, expression of AGER and MOK were significantly increased in patients with myositis compared to healthy controls (p< 0.05).

Conclusion: Overall, we observed increased RAGE expression in the skeletal muscle of myositis mice and human patients. These findings suggest that RAGE inhibition may be a promising strategy to dampen inflammation, improve muscle function, and ultimately enhance patient well-being. 

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/increased-rage-expression-in-myositis/