Temporal expression of heat shock proteins 60 and 70 at lesion-prone sites during atherogenesis in ApoE-deficient mice

Kanwar, Rupinder K., Kanwar, Jagat R., Wang, Dongmao, Ormrod, Douglas J. and Krissansen, Geoffrey W. 2001, Temporal expression of heat shock proteins 60 and 70 at lesion-prone sites during atherogenesis in ApoE-deficient mice, Arteriosclerosis thrombosis and vascular biology, vol. 21, no. 12, pp. 1991-1997.


Title Temporal expression of heat shock proteins 60 and 70 at lesion-prone sites during atherogenesis in ApoE-deficient mice
Author(s) Kanwar, Rupinder K.
Kanwar, Jagat R.
Wang, Dongmao
Ormrod, Douglas J.
Krissansen, Geoffrey W.
Journal name Arteriosclerosis thrombosis and vascular biology
Volume number 21
Issue number 12
Start page 1991
End page 1997
Total pages 7
Publisher Lippincott Williams & Wilkins
Place of publication Philadelphia, Pa.
Publication date 2001-12
ISSN 1079-5642
Keyword(s) atherosclerosis
heat shock proteins 60 and 70
apoE-deficient mice
aorta
Summary In the study, we investigate whether the expressions of heat shock protein (hsp)60 (a potential autoantigen) and the stress-inducible form of cytoprotector hsp70 are correlated with the development of atherosclerotic lesions in the aortic tree of apolipoprotein E–deficient (apoE-/-) mice. The apoE-/- mouse model is advantageous because the stress-inducible form of hsp70 is not constitutively expressed in mice, unlike primates; hence, tissues under stress can be clearly defined. Both mammalian hsps were detected newly expressed (before mononuclear cell infiltration) on aortic valves and endothelia at lesion-prone sites of 3-week-old apoE-/- mice. In 8- and 20-week-old mice, they were strongly and heterogeneously expressed in early to advanced fibrofatty plaques, with levels correlating with lesion severity. Expression was markedly downregulated in advanced collagenous, acellular, calcified plaques of 40- and 69-week-old mice and was absent in control aortas of normocholesterolemic wild-type (apoE+/+) mice. Western blot analysis of tissue homogenates confirmed the temporal expression of the hsps. Double immunostaining revealed that both hsps were expressed by lesional endothelial cells, macrophages, smooth muscle cells, and CD3+ T lymphocytes. This study provides evidence that hsp60 and hsp70 are temporally expressed on all major cell types in lesion-prone sites during atherogenesis, suggesting that few cells escape the toxic environment of the atherosclerotic plaque.
Language eng
Field of Research 110322 Rheumatology and Arthritis
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2001, American Heart Association, Inc.
Persistent URL http://hdl.handle.net/10536/DRO/DU:30026293

Document type: Journal Article
Collection: Institute of Biotechnology
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Created: Tue, 30 Mar 2010, 12:43:10 EST by Rupinder Kanwar

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