Collagen polymorphism in the normal and diseased blood vessel wall

Investigation of collagens types I, III and V
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      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 αA- and αB-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 αC-chain of type V collagen was detected in porcine but not human aorta.


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