Stephens H R, Duance V C, Dunn M J, Bailey A J, Dubowitz V
J Neurol Sci. 1982 Jan;53(1):45-62. doi: 10.1016/0022-510x(82)90079-x.
The striking proliferation of connective tissue characteristic of the muscular dystrophies can be attributed predominantly to an increase in endomysial and perimysial type III collagen. Carriers of muscular dystrophy occasionally revealed a slight increase in anti-type III collagen fluorescence, but no abnormalities in collagen disposition were observed in foetuses "at risk" for DMD. In contrast, the proportion of collagen types in neurogenic atrophies appeared normal although anti-type IV and V staining, which delineated the basement membrane, was very intense around atrophied fibres, as was also the case in small fibres in myopathic diseases. The detection of staining with anti-type III, IV and V collagens in splits which are sometimes observed in hypertrophied fibres in the muscular dystrophies supports the suggestion that abnormalities in collagen production, perhaps involving a defective modulation of myoblast-fibroblast expression, may be involved in the pathogenesis of these diseases.
肌营养不良症所特有的结缔组织显著增生,主要可归因于肌内膜和肌束膜III型胶原蛋白的增加。肌营养不良症携带者偶尔会出现抗III型胶原蛋白荧光略有增加的情况,但在患杜氏肌营养不良症“风险”胎儿中未观察到胶原蛋白分布异常。相比之下,神经源性萎缩中胶原蛋白类型的比例看似正常,尽管勾勒基底膜的抗IV型和V型染色在萎缩纤维周围非常强烈,肌病性疾病中的小纤维也是如此。在肌营养不良症肥大纤维中有时可见的分裂处检测到抗III型、IV型和V型胶原蛋白染色,这支持了以下观点:胶原蛋白产生异常,可能涉及成肌细胞-成纤维细胞表达的调节缺陷,可能参与了这些疾病的发病机制。