Abstract:
BACKGROUND:Cardiac allograft arteriosclerosis is a complex process of alloimmune response, chronic inflammation, and smooth muscle cell proliferation that includes cross talk between cytokines and growth factors. METHODS AND RESULTS:Our results in rat cardiac allografts established alloimmune response as an alternative stimulus capable of inducing vascular endothelial growth factor (VEGF) mRNA and protein expression in cardiomyocytes and graft-infiltrating mononuclear inflammatory cells, which suggests that these cells may function as a source of VEGF to the cells of coronary arteries. Linear regression analysis of these allografts with different stages of arteriosclerotic lesions revealed a strong correlation between intragraft VEGF protein expression and the development of intimal thickening, whereas blockade of signaling downstream of VEGF receptor significantly reduced arteriosclerotic lesions. In addition, in cholesterol-fed rabbits, intracoronary perfusion of cardiac allografts with a clinical-grade adenoviral vector that encoded mouse VEGF(164) enhanced the formation of arteriosclerotic lesions, possibly secondary to increased intragraft influx of macrophages and neovascularization in the intimal lesions. CONCLUSIONS:Our findings suggest a positive regulatory role between VEGF and coronary arteriosclerotic lesion formation in the allograft cytokine microenvironment.
journal_name
Circulationjournal_title
Circulationauthors
Lemström KB,Krebs R,Nykänen AI,Tikkanen JM,Sihvola RK,Aaltola EM,Häyry PJ,Wood J,Alitalo K,Ylä-Herttuala S,Koskinen PKdoi
10.1161/01.cir.0000016821.76177.d2subject
Has Abstractpub_date
2002-05-28 00:00:00pages
2524-30issue
21eissn
0009-7322issn
1524-4539journal_volume
105pub_type
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