Immunoproteasome subunit PSMB8 promotes skeletal muscle regeneration by regulating macrophage phenotyping switch in mice.
Abstract
Immunoproteasomes regulate the degradation of ubiquitin-coupled proteins and cell differentiation. However, its precise role in skeletal muscle regeneration remains unclear. In this study, we found that expression of the immunoproteasome subunit, PSMB8, increased significantly in young muscles after cardiotoxin-induced injury, whereas its expression was downregulated in injured aged mice. Genetic knockout or pharmacological inhibition of the immunoproteasome subunit, PSMB8, resulted in impaired muscle regeneration and increased interstitial fibrosis. PSMB8 inhibition by short interfering RNA (siRNA) or inhibitor decreased the differentiation ability of myoblasts. There was increased infiltration of inflammatory cells, especially Ly6C
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Research summary
The paper claims that the immunoproteasome subunit PSMB8 is crucial for skeletal muscle regeneration by influencing macrophage phenotyping. This research is relevant as it explores mechanisms that could potentially address age-related muscle degeneration, a significant aspect of aging.
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