Levels of MyoD protein expression following injury of mdx and normal limb muscle are modified by thyroid hormone

被引:26
作者
Anderson, JE
McIntosh, LM
Moor, AN
Yablonka-Reuveni, Z
机构
[1] Univ Manitoba, Dept Human Anat & Cell Sci, Winnipeg, MB R3E 0W3, Canada
[2] Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA
关键词
MyoD; muscle repair; mdx dystrophic mouse; thyroid hormone;
D O I
10.1177/002215549804600108
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Thyroid hormone (T3) affects muscle development and muscle regeneration. It also interacts with the muscle regulatory gene MyoD in culture and affects myoblast proliferation. We studied the localization of MyoD protein using a well-characterized polyclonal antibody for immunohistochemistry. Relative numbers of myogenic precursor cells per field were identified by their MyoD expression during muscle regeneration in normal and mdx dystrophic mice, with particular reference to the expression in mononuclear cells and myotubes at various T3 levels. In regeneration by normal muscles, relatively few MyoD(+) nuclei per field were present in mononuclear cells of euthyroid and hypothyroid mice. MyoD staining of mononuclear cell nuclei was approximately doubled in fields of regenerating muscles of normal hyperthyroid compared to euthyroid mice, and was observed in precursors that appeared to be aligned before fusion into myotubes. In mdx regenerating muscle, twofold more mononuclear cells positive for MyoD were present in all three treatment groups compared to normal muscles regenerating under the same condition Localization was similar to the pattern in normal euthyroid mice. However, in muscles regenerating in hyperthyroid mdx mice, both mononuclear cell nuclei and centrally located nuclei in a subpopulation (about 15%) of new myotubes formed after the crush injury were intensely stained for MyoD protein. The changes observed are consistent with reports on T3-induced alteration of muscle repair, and propose a link between MyoD regulation and the accelerated differentiation during regeneration under high T3 conditions.
引用
收藏
页码:59 / 67
页数:9
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