Myonucleus-Related Properties in Soleus Muscle Fibers of <i>mdx</i> Mice

Abstract

Distribution and total number of myonuclei in single soleus muscle fibers, sampled from tendon to tendon, were analyzed in mdx and wild-type (WT) mice. Apoptotic myonuclei and the microscopic structure around the myonuclei were also analyzed. Three types of muscle fibers of mdx mice with myonuclear distribution at either central, peripheral, or both central and peripheral regions were observed in the longitudinal analyses. All of the myonuclei were located at the peripheral region in WT mice. The total number of myonuclei counted in the whole length of fibers with peripheral myonuclei only was 17% less in mdx than in WT mice (p < 0.05). But the total myonuclear numbers in mdx mouse fibers with different distribution (peripheral vs. central) of myonuclei were identical, and the peripheral nucleus was noted where the central nucleus was missing. Myonuclei located between the center and peripheral regions were also seen in the cross-sectional analyses of muscle fibers. The cross-sectional area and length of fibers, sarcomere number, myonuclear size, myosin heavy chain expression, satellite cell number and neuromuscular junction were identical between each type of fiber. Apoptosis was not detected in any myonuclei located either in central or peripheral regions of muscle fibers. Thus, it was suggested that apoptosis-related loss of central myonuclei and regeneration-related new accretion at the peripheral region is not the cause of different distribution of myonuclei seen in muscle fibers in mdx mice. However, it was speculated that cross-sectional migration of myonuclei from central to peripheral regions may be induced in response to regeneration, because the total myonuclear numbers in fibers with different distribution of myonuclei were identical, and the peripheral nucleus was noted where the central nucleus was missing. Further, myonuclei located between the center and peripheral regions were also seen. However, the question remains as to how or why nuclei might migrate to the periphery in a regenerating muscle fiber, since there was no microscopic evidence of any structural changes around the myonuclei that may be responsible for the movement of the nucleus.

Macrophage deficiency in osteopetrotic (op/op) mice inhibits activation of satellite cells and prevents hypertrophy in single soleus fibers

“…Exposure to microgravity or hind limb unloading of rodents causes passive shortening of soleus muscle due to ankle plantarflexion (20,39,59), which reduces the mechanical stress (20) and neural activity (19,20,39,43). Even though it is well-reported that muscles composed predominantly of slowtwitch fibers are more susceptible to unloading-related atrophy (6,41,42,(45)(46)(47)59), atrophy in soleus muscle of mice composed of fast-twitch fibers mainly was also observed in all types of mice, as was reported elsewhere (40,48,55). The unloading-related decreases in fiber length and sarcomere number may be associated with the remodeling of muscle fibers and sarcomeres, as was reported before (20,59).…”

“…The muscles were stored in a cellbanker (Nihon Zenyaku, Tokyo, Japan) at Ϫ80°C until analyzed, as was reported previously (41,55,59). The muscles stored in the cellbanker were thawed instantly at 35°C.…”

Changes in Aging Mouse Neuromuscular Junctions Are Explained by Degeneration and Regeneration of Muscle Fiber Segments at the Synapse

“…Interestingly, not only did all the fibers with newly fragmented junctions (those with weak first color and strong second color) have central nuclei underneath the NMJ, 4% of the older fragmented junctions (those with strong first color, strong second color) did as well. That the majority of the fragmented junctions did not have fibers with central nuclei in the synaptic region suggests that either these fragmented junctions were not generated as a result of degeneration and regeneration or that the central nuclei, with time, migrate to the periphery in regenerated fibers, a subject of some controversy in the literature (Jirmanová and Thesleff, 1972; Duchen et al, 1974; Schmalbruch, 1976; Couteaux et al, 1988; Karpati et al, 1988; Rich and Lichtman, 1989; Terada et al, 2010). …”

Opposing microtubule motors drive robust nuclear dynamics in developing muscle cells

“…During fiber repair, myogenic cells fuse with the injured fiber, contributing a new nucleus (Chargé and Rudnicki, 2004). These nuclei are positioned at the periphery of the myofiber (Rich and Lichtman, 1989;Terada et al, 2010;Li et al, 2011), and it is likely that both nuclear translocation and rotation are required for this positioning. In diseases like the muscular dystrophies, where mechanically induced muscle damage occurs frequently, nuclear dynamics may be essential for proper fiber repair and subsequent muscle function.…”