Active Remodeling of the Coronary Arterial Lesions in the Late Phase of Kawasaki Disease
- 27 June 2000
- journal article
- other
- Published by Wolters Kluwer Health in Circulation
- Vol. 101 (25) , 2935-2941
- https://doi.org/10.1161/01.cir.101.25.2935
Abstract
Background —Remodeling of the coronary artery lesions in Kawasaki disease has been observed in longitudinal angiographic studies. However, mechanisms of such remodeling have not yet been elucidated. Methods and Results —We examined formalin-fixed specimens of the coronary arteries immunohistochemically by using antibodies against vascular growth factors (GFs) and their receptors in 7 children with Kawasaki disease, 9 children with no coronary disease, and 3 adults with atherosclerosis. In the thickened intima at stenotic sites and at recanalized vessels with Kawasaki disease, extensive expression of vascular GFs, such as transforming GF-β 1 , platelet-derived GF-A, and basic fibroblast GF, was observed both within and surrounding smooth muscle cells. Vascular endothelial GF was observed within smooth muscle cells. Furthermore, all of these GFs were strongly expressed in the newly formed microvessels within the intima. In the thinned media, these GFs were focally and weakly expressed. In contrast, these GFs were expressed only in the media in the control children. In cases of adult atherosclerosis, GFs were expressed diffusely in the media but focally and weakly if at all in the intima. Conclusions —Active remodeling of the coronary artery lesions in Kawasaki disease continues in the form of luxuriant intimal proliferation and neoangiogenesis for several years after the onset of the disease. This process is distinct from adult-onset atherosclerosis.Keywords
This publication has 12 references indexed in Scilit:
- Functional behavior and morphology of the coronary artery wall in patients with Kawasaki disease assessed by intravascular ultrasoundJournal of the American College of Cardiology, 1996
- Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1.Journal of Clinical Investigation, 1995
- Fluid shear stress induces endothelial transforming growth factor beta-1 transcription and production. Modulation by potassium channel blockade.Journal of Clinical Investigation, 1995
- Clinical significance of morphologic classification of coronary arterial segmental stenosis due to Kawasaki diseaseThe American Journal of Cardiology, 1993
- Expression of transforming growth factor-beta 1 is increased in human vascular restenosis lesions.Journal of Clinical Investigation, 1992
- Role of PDGF-A expression in the control of vascular smooth muscle cell growth by transforming growth factor-beta.The Journal of cell biology, 1990
- Release of basic fibroblast growth factor-heparan sulfate complexes from endothelial cells by plasminogen activator-mediated proteolytic activity.The Journal of cell biology, 1990
- Inhibition of endothelial cell movement by pericytes and smooth muscle cells: activation of a latent transforming growth factor-beta 1-like molecule by plasmin during co-culture.The Journal of cell biology, 1989
- Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells.Journal of Clinical Investigation, 1989
- Follow-up study of coronary artery lesions due to Kawasaki disease by serial selective coronary arteriography in 200 patientsHeart and Vessels, 1987