Morton L F, Barnes M J
Atherosclerosis. 1982 Mar;42(1):41-51. doi: 10.1016/0021-9150(82)90124-1.
Estimation of collagens types I and III in pepsin digests and by analysis of specific cyanogen-bromide derived peptides by SDS-polyacrylamide gel electrophoresis, has indicated that both the undiseased human aortic media and the atherosclerotic plaque of the diseased intima contain more type I collagen than type III. There was only a relatively small shift in composition in favour of type I collagen in the diseased compared to the undiseased tissue. Diffusely thickened intima was similar in composition to the atherosclerotic plaque. These results suggest that both atherogenesis and diffuse intimal thickening may involve primarily smooth muscle cell hyperplasia with increased overall collagen production but little alteration in cell phenotype as regards the relative proportions of the individual collagens produced. They do not support the contention that atherosclerosis involves a 'transformation' of smooth muscle cells to fibroblast in type, whereby a major switch in synthesis occurs from largely type III collagen to mainly type I in disease. Type V collagen(s) containing both alpha A- and alpha B-chains has been detected throughout the vessel wall in diffusely thickened intima, media and adventitia, as well as in the plaque where, in the latter case, a marked enrichment relative to interstitial collagens was noted. This is presumed to reflect the relatively cellular nature of the atherosclerotic lesion. The alpha C-chain of type V collagen was detected in porcine but not human aorta.
通过对胃蛋白酶消化产物进行I型和III型胶原蛋白的评估,并利用十二烷基硫酸钠-聚丙烯酰胺凝胶电泳对特定溴化氰衍生肽进行分析,结果表明,未患病的人体主动脉中膜和患病内膜的动脉粥样硬化斑块中,I型胶原蛋白均多于III型胶原蛋白。与未患病组织相比,患病组织中胶原蛋白组成仅出现相对较小的偏向I型胶原蛋白的变化。弥漫性增厚的内膜在组成上与动脉粥样硬化斑块相似。这些结果表明,动脉粥样硬化形成和弥漫性内膜增厚可能主要涉及平滑肌细胞增生,导致整体胶原蛋白生成增加,但就所产生的各型胶原蛋白的相对比例而言,细胞表型几乎没有改变。它们并不支持动脉粥样硬化涉及平滑肌细胞向成纤维细胞的“转化”这一观点,即在疾病状态下,合成过程会从主要的III型胶原蛋白大幅转变为主要的I型胶原蛋白。在弥漫性增厚的内膜、中膜和外膜以及斑块的整个血管壁中均检测到含有αA链和αB链的V型胶原蛋白,在后一种情况下,相对于间质胶原蛋白,V型胶原蛋白显著富集。据推测,这反映了动脉粥样硬化病变相对细胞化的性质。在猪主动脉中检测到了V型胶原蛋白的αC链,但在人体主动脉中未检测到。