Pathology of atheromatous lesions in inbred and genetically engineered mice. Genetic determination of arterial calcification.

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Abstract
We report comprehensive pathological studies of atheromatous lesions in various inbred mouse strains fed a high-fat, high-cholesterol diet and in two genetically engineered strains that develop spontaneous lesions on a low-fat chow diet. Coronary and aortic lesions were studied with respect to anatomic locations, lesion severity, calcification, and lipofuscin deposition. Surprisingly, the genetic determinants for coronary fatty lesion formation differed in part from those for aortic lesion development. This suggests the existence of genetic factors acting locally as well as systematically in lesion development. We used immunohistochemical analyses to determine the cellular and molecular compositions of the lesions. The aortic lesions contained monocyte/macrophages, lipid, apolipoprotein B, serum amyloid A proteins, and immunoglobulin M and showed expression of vascular cell adhesion molecule-1 and tumor necrosis factor-alpha, all absent in normal arteries. In certain strains, advanced lesions developed in...