PGC-1α-b overexpression significantly improved maximum isometric torque recovery and reduced muscle damage markers after eccentric contraction in mice.
Does PGC-1α-b overexpression prevent eccentric contraction-induced muscle injury in mice?
PGC-1α-b overexpression protects against eccentric contraction-induced muscle damage through a utrophin-independent mechanism in mice.
Absolute Event Rate: 0% vs 0%
Abstract Slower oxidative fibers are more resistant to eccentric contraction (ECC)‐induced muscle damage than fast‐twitch glycolytic fibers, but the mechanisms remain unclear. This study investigated the roles of the exercise‐inducible PGC‐1α isoform PGC‐1α‐b and utrophin in protecting against ECC‐induced damage. ECCs were induced by supramaximal electrical stimulation of the left triceps surae in C57BL/6N wild‐type (WT), PGC‐1α‐b transgenic (Tg), utrophin knockout (Utrn KO), and PGC‐1α‐b Tg/Utrn KO mice. Although the proportion of fast‐type myosin heavy chain (MyHC) IIb in the gastrocnemius muscle was modestly lower in PGC‐1α‐b Tg and PGC‐1α‐b Tg/Utrn KO mice than in WT and Utrn KO mice, MyHC IIb remained the predominant isoform. At 3 days post injury (dpi), WT and Utrn KO mice exhibited reduced maximum isometric torque (MIT), Evans blue dye (EBD) staining in MyHC IIb‐positive fibers, and calpain‐1 activation. In contrast, PGC‐1α‐b Tg and PGC‐1α‐b Tg/Utrn KO mice showed substantial MIT recovery at 1 dpi and minimal EBD uptake and calpain‐1 activation at 3 dpi. PGC‐1α‐b Tg muscles also preserved excitation‐contraction coupling proteins and displayed increased mitochondrial markers and integrin α7B expression. Together, our findings suggest that PGC‐1α‐b confers resistance to ECC‐induced muscle damage through a Utrn‐independent mechanism.
Naito et al. (Thu,) reported a other. PGC-1α-b overexpression significantly improved maximum isometric torque recovery and reduced muscle damage markers after eccentric contraction in mice.