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Low-grade chronic inflammation in regions of the normal mouse arterial intima predisposed to atherosclerosis.
J Exp Med. 2006 Sep 4; 203(9):2073-83
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15 Aug 2006
Confirmation, New Finding, Technical Advance
DOI: 10.3410/f.1033751.387948
This is the first study comparing gene and protein expression in the aortic vessel wall (not just endothelial cells) in areas of laminar and disturbed flow in a relevant mouse model.
A surprisingly robust difference is found in the mRNA and protein abundance of CD11c, suggesting that dendritic cells...Continue reading
A surprisingly robust difference is found in the mRNA and protein abundance of CD11c, suggesting that dendritic cells...Continue reading
This is the first study comparing gene and protein expression in the aortic vessel wall (not just endothelial cells) in areas of laminar and disturbed flow in a relevant mouse model.
A surprisingly robust difference is found in the mRNA and protein abundance of CD11c, suggesting that dendritic cells are present in areas of disturbed but not laminar flow.
A surprisingly robust difference is found in the mRNA and protein abundance of CD11c, suggesting that dendritic cells are present in areas of disturbed but not laminar flow.
Disclosures
None declared
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Ley K: F1000Prime Recommendation of [Jongstra-Bilen J et al., J Exp Med 2006, 203(9):2073-83]. In F1000Prime, 15 Aug 2006; DOI: 10.3410/f.1033751.387948. F1000Prime.com/1033751#eval387948
F1000Prime Recommendations, Dissents and Comments for [Jongstra-Bilen J et al., J Exp Med 2006, 203(9):2073-83]. In F1000Prime, 23 May 2013; F1000Prime.com/1033751
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Atherosclerotic lesions develop in regions of arterial curvature and branch points, which are exposed to disturbed blood flow and have unique gene expression patterns. The cellular and molecular basis for atherosclerosis susceptibility in these regions is not completely understood. In the intima of atherosclerosis-predisposed regions of the wild-type C57BL/6 mouse aorta, we quantified increased expression of several proinflammatory genes that have been implicated in atherogenesis, including vascular cell adhesion molecule-1 (VCAM-1) and a relative abundance of dendritic cells, but only occasional T cells. In contrast, very few intimal leukocytes were detected in regions resistant to atherosclerosis; however, abundant macrophages, including T cells, were found throughout the adventitia (Adv). Considerably lower numbers of intimal CD68+ leukocytes were found in inbred atherosclerosis-resistant C3H and BALB/c mouse strains relative to C57BL/6 and 129; however, leukocyte distribution throughout the Adv of all strains was similar. The predominant mechanism for the accumulation of intimal CD68+ cells was continued recruitment of bone marrow-derived blood monocytes, suggestive of low-grade chronic inflammation. Local proliferation of intimal leukocytes was low. Intimal CD68+ leukocytes were reduced in VCAM-1-deficient mice, suggesting that mechanisms of leukocyte accumulation in the intima of normal aorta are analogous to those in atherosclerosis.
DOI: 10.1084/jem.20060245
PMID: 16894012
