Changes in Mass and Performance in Rabbit Muscles after Muscle Damage with or without Transplantation of Primary Satellite Cells

• Published in: Cell transplantation 2002-01, Vol.11 (2), p.169-180
• Main Authors: Andalousi, Ramzi Boubaker El, Daussin, Paul-André, Micallef, Jean-Paul, Roux, Colette, Nougues, Jean, Chammas, Michel, Reyne, Yves, Bacou, Francis
• Format: Article
• Language: English
• Subjects: Animals; Cells, Cultured; Computer Science; Energy Metabolism - physiology; Gene Expression - physiology; Graft Survival - physiology; Life Sciences; Male; Muscle Contraction - physiology; Muscle Fibers, Skeletal - cytology; Muscle Fibers, Skeletal - physiology; Muscle, Skeletal - injuries; Muscle, Skeletal - physiopathology; Muscle, Skeletal - surgery; Muscular Diseases - pathology; Muscular Diseases - physiopathology; Muscular Diseases - surgery; Myoblasts, Skeletal - cytology; Myoblasts, Skeletal - physiology; Myoblasts, Skeletal - transplantation; Myosin Heavy Chains - genetics; Myosin Heavy Chains - metabolism; Organ Size - physiology; Protein Isoforms - genetics; Protein Isoforms - metabolism; Rabbits; Recovery of Function - physiology; Regeneration - physiology; RNA, Messenger - metabolism
• ISSN: 0963-6897; 1555-3892
• DOI: 10.3727/096020198389898

Changes in morphology, metabolism, myosin heavy chain gene expression, and functional performances in damaged rabbit muscles with or without transplantation of primary satellite cells were investigated. For this purpose, we damaged bilaterally the fast muscle tibialis anterior (TA) with either 1.5 or 2.6 ml cardiotoxin 10–5 M injections. Primary cultures of satellite cells were autotransplanted unilaterally 5 days after muscle degeneration. Two months postoperation, the masses of damaged TAs, with or without transplantation, were significantly larger than those of the controls. Furthermore, damaged transplanted muscles weighed significantly more than damaged muscles only. The increase in muscle mass was essentially due to increased fiber size. These results were independent of the quantity of cardiotoxin injected into the muscles. Maximal forces were similar in control and 2.6 ml damaged TAs with or without satellite cell transfer. In contrast, 1.5 ml damaged TAs showed a significant decrease in maximal forces that reached the level of controls after transplantation of satellite cells. Fatigue resistance was similar in control and 1.5 ml damaged TAs independently of satellite cell transfer. Fatigue index was significantly higher in 2.6 ml damaged muscles with or without cell transplantation. These changes could be explained in part by muscle metabolism, which shifted towards oxidative activities, and by gene expression of myosin heavy chain isoforms, which presented an increase in type IIa and a decrease in type I and IIb in all damaged muscles with or without cell transfer. Under our experimental conditions, these results show that muscle damage rather than satellite cell transplantation changes muscle metabolism, myosin heavy chain isoform gene expression, and, to a lesser extent, muscle contractile properties. In contrast, muscle weight and fiber size are increased both by muscle damage and by satellite cell transfer.