Byron Craig D, Hamrick Mark W, Wingard Christopher J
Department of Surgery, CJ-1117, Medical College of Georgia, 1120, 15th Street, Augusta, GA 30912, USA.
Arch Oral Biol. 2006 May;51(5):396-405. doi: 10.1016/j.archoralbio.2005.09.006. Epub 2005 Nov 2.
Myostatin (GDF8) and dystrophin are critical molecules for muscle organisation. Myostatin is involved in regulating muscle growth and development, whereas dystrophin is part of the dystrophin-glycoprotein complex (DGC), which anchors the cytoskeleton to the sarcolemma. We examined temporalis muscle morphology and function in myostatin deficient and dystrophin deficient (Mdx) mice in order to determine how myostatin and dystrophin affect bite force and muscle fibre composition. Bite forces from 4-month-old myostatin-/-, dystrophin deficient (Mdx) and normal control mice were measured by load cell and field stimulation of the temporalis muscle. Tissue sections were stained with haemotoxylin and eosin (H&E) and the periodic acid-Schiff reaction (PAS) to assess morphology and fibre type differences. A positive relationship between bite force and muscle mass for both genetic models was observed. Both Mstn-/- and Mdx mice showed significant elevation in bite force and muscle mass. Histological examination revealed greater muscle fibre cross-sectional area variability in Mdx mice (ANOVA, F=5.6, P<0.01). Surprisingly, the Mstn-/- mice demonstrated a disproportionate increase in bite force at higher stimulation frequencies with comparison of regression lines for force-frequency data (ANOVA, F=3.46, P<0.07). Muscle fibre typing using a PAS staining technique revealed significantly more type IIx/b glycolytic muscle fibres in the Mstn-/- mice. Our results suggest that histopathologies associated with Mdx mice did not diminish gross temporalis structure or function, whilst the force-frequency changes associated with Mstn-/- mice were reflected in an elevation of type IIx/b fibres.
肌生成抑制素(生长分化因子8)和肌营养不良蛋白是肌肉组织的关键分子。肌生成抑制素参与调节肌肉生长和发育,而肌营养不良蛋白是肌营养不良蛋白-糖蛋白复合物(DGC)的一部分,该复合物将细胞骨架锚定到肌膜。我们研究了肌生成抑制素缺陷和肌营养不良蛋白缺陷(Mdx)小鼠的颞肌形态和功能,以确定肌生成抑制素和肌营养不良蛋白如何影响咬合力和肌纤维组成。通过测力传感器和颞肌的场刺激测量了4个月大的肌生成抑制素基因敲除小鼠、肌营养不良蛋白缺陷(Mdx)小鼠和正常对照小鼠的咬合力。组织切片用苏木精和伊红(H&E)染色以及过碘酸希夫反应(PAS)染色,以评估形态和纤维类型差异。在两种遗传模型中均观察到咬合力与肌肉质量之间呈正相关。Mstn-/-和Mdx小鼠的咬合力和肌肉质量均显著升高。组织学检查显示,Mdx小鼠的肌纤维横截面积变异性更大(方差分析,F=5.6,P<0.01)。令人惊讶的是,与力-频率数据的回归线相比,Mstn-/-小鼠在较高刺激频率下咬合力增加不成比例(方差分析,F=3.46,P<0.07)。使用PAS染色技术进行的肌纤维分型显示,Mstn-/-小鼠中IIx/b型糖酵解肌纤维明显更多。我们的结果表明,与Mdx小鼠相关的组织病理学并未损害颞肌的总体结构或功能,而与Mstn-/-小鼠相关的力-频率变化反映在IIx/b型纤维的增加上。