Untitled

Abstract

We previously showed that satellite cells isolated from rabbit fast-twitch and slow-twitch muscles presented different behaviours in culture; cells from slow muscle differentiated more quickly and fused into more numerous myotubes than those from fast muscle. Moreover, only slow-muscle derived satellite cells expressed in vitro the slow type I myosin heavy chain isoform (MyHC). We wanted to investigate whether the properties of satellite cells originating from different muscles were under the influence of the adult fibre type on which they were located. For this purpose, we transformed the properties of the adult rabbit fast-twitch semimembranosus accessorius (SMa; approximately 100% type II fibres) and the slow-twitch semimembranosus proprius (SMp; 100% type I fibre) muscles by (1) cross-reinnervating the SMp with the main branch of the fast SMa nerve; or (2) electrical stimulation at 10 Hz of the SMa muscle. We studied their satellite cells in vitro. Five-month cross-reinnervation of the SMp induced a large shift of its MyHC type characteristics towards those of a fast muscle, and three-month electrical stimulation at low frequency transformed the fast-twitch SMa into a slow-twitch muscle, as shown by SDS-PAGE of MyHC. In spite of the transformation of their muscle characteristics, satellite cells in culture kept their original properties. Indeed, as shown by MyoD and myogenin gene expression as markers of fusion, satellite cells isolated from cross-reinnervated and from control SMp began to fuse by eight days of culture, and expressed MyoD and myogenin at that stage. Later they differentiated into numerous myotubes. Satellite cells isolated from electrically stimulated and control SMa presented a similar behaviour in culture: they did not express MyoD and myogenin at eight days, and fused by ten days into only a few myotubes. Moreover, MyHC gene expression showed that, in contrast with slow-muscle derived satellite cells, the type I MyHC gene was not expressed by satellite cells isolated from the stimulated SMa in spite of its homogeneous type I fibre composition. Taken together, these data support the idea that once constituted, muscle fibre types per se do not influence the properties of their associated satellite cells.

Interactions between β-enolase and creatine kinase in the cytosol of skeletal muscle cells

“…Rabbit satellite cells were cultured as described previously [20] from semimembranosus proprius, a slow-twitch muscle [21]. Satellite cells were isolated by digestion of muscle fibres with pronase [20,21]. The isolated cells were grown in dishes 6 cm in diameter, the bases of which had been replaced with sealed glass coverslips to allow microscopic observation.…”

Immunoneutralization of TGFβ1 Improves Skeletal Muscle Regeneration: Effects on Myoblast Differentiation and Glycosaminoglycan Content

“…Several studies, including our previous works [13, 15–17], have reported that myoblasts isolated from fast or slow muscles and grown in vitro display some differential growth and differentiation properties. The differences of myoblasts from fast and slow muscles are maintained independently of the phenotypic transition of muscle fibers induced by an adequate chronic electrical stimulation.…”

Skeletal Muscle Metabolic Alternation Develops Sarcopenia

“…In the study of skeletal muscle transplantation in rodents, it was found that the ability of muscle regeneration depends more on the age of the host, indicating that microenvironmental changes are one of the important factors for the decline of skeletal muscle SCs function [ 58 ]. The SCs from soleus were transplanted into the extensor digitorum long muscle, and slow-twitch muscle fibers were observed after 3 months [ 59 ]. However, this phenomenon was not observed after 6 months, suggesting that the skeletal muscle metabolic microenvironment can effectively reprogram mature regenerated myofibers, but not the SCs themselves.…”

“…However, this phenomenon was not observed after 6 months, suggesting that the skeletal muscle metabolic microenvironment can effectively reprogram mature regenerated myofibers, but not the SCs themselves. Many studies have found that changes in myofiber metabolism after stimulation by oxidative or glycolysis, respectively, indicating that SCs are malleable [ 59 , 60 ]. The above studies confirmed that changes in skeletal muscle microenvironment caused a decrease in SCs content, which may be a key factor causing fast-twitch oxidized myofiber atrophy leading to sarcopenia.…”