Skeletal muscle has an ability to regenerate in response to injury due to the presence of
satellite cells. Injury in skeletal muscle causes infiltration of pro-inflammatory
macrophages (M1 macrophages) to remove necrotic myofibers, followed by their
differentiation into anti-inflammatory macrophages (M2 macrophages) to terminate the
inflammation. Since both M1 and M2 macrophages play important roles, coordinated
regulation of their kinetics is important to complete muscle regeneration successfully.
Progranulin (PGRN) is a pluripotent growth factor, having a protective role against the
inflamed tissue. In the central nervous system, PGRN regulates inflammation by inhibiting
the activation of microglia. Here we used muscle injury model of PGRN-knockout (PGRN-KO)
mice to elucidate whether it has a role in the kinetics of macrophages during muscle
regeneration. We found the prolonged persistence of macrophages at the late phase of
regeneration in PGRN-KO mice, and these macrophages were suggested to be M2 macrophages
since this was accompanied with an increased CD206 expression. We also observed muscle
hypertrophy in PGRN-KO mice at the late stage of muscle regeneration. Since M2 macrophages
are known to have a role in maturation of myofibers, this muscle hypertrophy may be due to
the presence of increased number of M2 macrophages. Our results suggest that PGRN plays a
role in the regulation of kinetics of macrophages for the systemic progress of muscle
regeneration.
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