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首页> 外文期刊>Folia histochemica et cytobiologica >Caveolin-1, caveolin-3 and VEGF expression in the masticatory muscles of mdx mice
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Caveolin-1, caveolin-3 and VEGF expression in the masticatory muscles of mdx mice

机译：mdx小鼠咀嚼肌中的Caveolin-1，caveolin-3和VEGF表达

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摘要

Duchenne muscular dystrophy (DMD) and murine X-linked muscular dystrophy (mdx), its murine model, are characterized by muscle damage and muscle weakness associated with inflammation and new vessel formation. Caveolins, dystrophin-associated proteins, are involved in the pathogenesis of DMD, because increased numbers of caveolae are found in DMD and mdx hindlimb muscles. Caveolae influence angiogenesis due to their content of vascular endothelial growth factor (VEGF) receptors. Orofacial muscles in mdx mice undergo muscle necrosis followed by muscle regeneration. To ascertain the role of caveolins and VEGF in the pathogenesis of dystrophic masticatory muscles, we examined the expression of caveolin-1 (cav-1), caveolin-3 (cav-3) and VEGF in control and mdx mice. In mdx masticatory muscles, no changes in transcript and protein levels of VEGF were found, whereas cav-1 and cav-3 expression was increased. Using immunohistochemistry, a strong sarcolemmal staining of caveolin-3 in regenerated muscle fibers was found. Furthermore, immunohistochemistry with the caveolin-1 antibody showed an increase in the amount of blood vessels in areas with regenerating muscle fibers. Dystrophic masticatory muscles showed changes comparable to those of hindlimb muscles in the expression of cav-1 and cav-3. The angiogenesis seems to be unaffected in the jaw muscles of mdx mice. We speculate that the increased caveolin expression could cause extensive and efficient muscle regeneration.
机译：Duchenne肌营养不良症（DMD）和鼠X连锁肌营养不良症（mdx）是其鼠类模型，其特征是与炎症和新血管形成相关的肌肉损伤和肌肉无力。小窝蛋白，与肌营养不良蛋白相关的蛋白质，参与了DMD的发病机理，因为在DMD和mdx后肢肌肉中发现了小窝的数量增加。由于它们的血管内皮生长因子（VEGF）受体含量，小窝影响血管生成。 mdx小鼠的口面部肌肉会发生肌肉坏死，然后发生肌肉再生。为了确定caveolins和VEGF在营养不良性咀嚼肌发病机理中的作用，我们检查了cavolin-1（cav-1），caveolin-3（cav-3）和VEGF在对照和mdx小鼠中的表达。在mdx咀嚼肌中，未发现VEGF的转录本和蛋白质水平发生变化，而cav-1和cav-3的表达增加。使用免疫组织化学，在再生的肌肉纤维中发现了caveolin-3的强烈肌膜染色。此外，用caveolin-1抗体进行的免疫组织化学分析显示，肌肉纤维再生区域的血管数量增加。营养不良的咀嚼肌在cav-1和cav-3的表达方面具有与后肢肌肉相当的变化。血管生成似乎在mdx小鼠的下颌肌肉中不受影响。我们推测增加的小窝蛋白表达可能引起广泛而有效的肌肉再生。

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