THE EFFECTS OF HYPERTHYROIDISM ON MUSCULAR-DYSTROPHY IN THE MDX MOUSE - GREATER DYSTROPHY IN CARDIAC AND SOLEUS MUSCLE
THE EFFECTS OF HYPERTHYROIDISM ON MUSCULAR-DYSTROPHY IN THE MDX MOUSE - GREATER DYSTROPHY IN CARDIAC AND SOLEUS MUSCLE
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DOI：
10.1002/mus.880170109
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发表时间：
1994-01-01
期刊：
影响因子：
3.4
通讯作者：
KARDAMI, E
中科院分区：
文献类型：
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作者：
ANDERSON, JE;LIU, L;KARDAMI, E
用三碘甲状腺原氨酸（T-3）治疗mdx小鼠14天，观察其肌肉损伤及修复情况。检查后肢和心肌营养不良的严重程度、肌肉中心化程度和纤维大小。对照组和mdx小鼠在T-3治疗后出现心肌肥大和骨骼肌萎缩。在T-3治疗的mdx小鼠中，心脏和比目鱼肌（但不是快速抽搐）都有更大、更频繁的营养不良病变，并且在T-3治疗后mdx比目鱼肌的新肌管面积增加。过量的T-3可能延迟mdx小鼠的骨骼肌形成，这可能与甲状腺功能亢进小鼠碱性成纤维细胞生长因子染色普遍减少有关。这是第一次观察到代谢扰动会恶化mdx营养不良，并可能以肌肉特异性的方式进行修复，并且可能与t -3诱导的肌球蛋白重链表达的变化以及肌营养不良蛋白缺乏肌肉的机械应变增加有关。(C) 1994 John Wiley and Sons, Inc。
Muscle damage and repair were studied in mdx mice treated with triiodothyronine (T-3) for 14 days. Hindlimb and cardiac muscles were examined for the severity of dystrophy, the degree of muscle centronucleation, and fiber size. In control and mdx mice, cardiac hypertrophy and skeletal muscle atrophy were present after T-3 treatment. Both cardiac and soleus (but not fast-twitch) muscles had larger, more frequent dystrophic lesions in T-3-treated mdx mice, and mdx soleus had an increased area of new myotubes after T-3. Skeletal myogenesis in mdx mice may have been delayed by excess T-3, possibly related to the general reduction in staining for basic fibroblast growth factor in hyperthyroid mice. These are the first observations of a metabolic perturbation which worsens mdx dystrophy and possibly repair in a muscle-specific manner, and are likely related to T-3-induced changes in myosin heavy chain expression, and to increased mechanical strain on dystrophin-deficient muscles. (C) 1994 John Wiley and Sons, Inc.