Endogenous Galectin-3 is Required for Skeletal Muscle Repair

摘要: ABSTRACT Skeletal muscle has the intrinsic ability to self-repair through a multifactorial process, but many aspects of its cellular and molecular mechanisms are not fully understood. There is increasing evidence that some members mammalian β-galactoside-binding protein family (galectins) involved in muscular repair process (MRP), including galectin-3 (Gal-3). However, there questions about role this on self-repair. Here, we demonstrate endogenous Gal-3 required for: i) vivo using chloride-barium myolesion mouse model, ii) primary myoblasts myogenic programming. Injured from knockout mice (GAL3KO) showed persistent inflammation associated with compromised formation fibrotic tissue lesion site. In GAL3KO mice, osteopontin expression remained high even after 7 14 days myolesion, while MyoD myogenin had decreased their expression. myoblast cell culture, Pax7 detection seems sustain when cells stimulated differentiation drastically reduced. These findings suggest temporal levels these transcriptional factors appear be altered Gal-3-deficient culture compared Wild Type (WT) cells. We observed WT states, both vitro, sarcoplasm/cytoplasm myonuclei; as proceeds, reduced, location confined sarcolemma/plasma membrane. also change temporal-spatial profile transcription during myolesion. Overall, results for skeletal process.