Role of mast cell chymase in excessive wound-healing response to vascular injury.
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概要
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This study has analyzed the pathogenetic mechanism of the intimal thickening after baloon injury, which is currently a serious problem on the balloon angioplasty for coronary arteriosclerosis, from the aspect of wound-healing inflammation. The locally generated angiotensin II (AII), which is known for its aggravating effect on vascular hypertrophy, has been implicated to participate in the pathogenic mechanism. One month after the balloon injury, dog arteries showed myointimal hyperplasia as well as the increases in AII and AII-generating enzymes, angiotensin-converting enzyme and mast cell chymase, with the latter enzyme increasing more markedly. In the adventitia of lesioned vessels, the density of mast cells and fibrolasts was increased with apparent fibrosis and angiogenesis. These pathohistological findings suggest that the adventitial fibrosis reflects an excessive woundhealing response to the injury, and that the mast cell-fibroblast cross-talk may couple the adventitial fibrosis with the intimal hyperplasia. In this hyperplastic lesion, mast cell chymase seems to play a pivotal role by generating AII, and also by chymase's proinflammatory actions which are not yet fully defined. Thus, it is reasonable to regard the intimal thickening as a manifestation of exaggerated wound-healing response to an injury.
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