4.4 Article

Alterations of temporalis muscle contractile force and histological content from the myostatin and Mdx deficient mouse

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ARCHIVES OF ORAL BIOLOGY
卷 51, 期 5, 页码 396-405

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.archoralbio.2005.09.006

关键词

skeletal muscle; bite force; GDF8; dystrophin; temporalis

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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 toad 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. (c) 2005 Elsevier Ltd. All rights reserved.

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