David P. Hajjar
Cornell University
177 Papers
2.7K Citations
David P. Hajjar is an academic researcher from Cornell University. The author has contributed to research in topics: Cholesteryl ester & Cholesterol. The author has an hindex of 58, co-authored 176 publications. Previous affiliations of David P. Hajjar include National Institutes of Health & University of New Hampshire.
Chat about Author
Papers
Recombinant glutathione S-transferase/CD36 fusion proteins define an oxidized low density lipoprotein-binding domain.
S. F. A. Pearce,P. Roy,Andrew C. Nicholson,David P. Hajjar,Maria Febbraio,Roy L. Silverstein +5 more
TL;DR: This study demonstrates unique regions of the scavenger receptor CD36 that bind the Ox-LDL ligand and provides information as to potential control of the trafficking of modified lipoproteins into the blood vessel wall.
•Journal Article
Herpesvirus infection enhances cholesterol and cholesteryl ester accumulation in cultured arterial smooth muscle cells.
TL;DR: The hypothesis that lipid accumulation in arteries of normocholesterolemic chickens may result from MDV infection acting at the cellular level to induce lipid accumulation that resembles that in human atheroarteriosclerosis is supported.
Induction of CD36 expression by oxidized LDL and IL-4 by a common signaling pathway dependent on protein kinase C and PPAR-γ
Jianwei Feng,Jihong Han,S. Freida A. Pearce,Roy L. Silverstein,Antonio M. Gotto,David P. Hajjar,Andrew C. Nicholson +6 more
TL;DR: Evaluated signaling pathways involved in the induction of CD36 demonstrate that two divergent physiological or pathophysiological agonists utilize a common pathway to up-regulate ofCD36 gene expression.
Transforming growth factor-beta up-regulates low density lipoprotein receptor-mediated cholesterol metabolism in vascular smooth muscle cells.
TL;DR: The effects of transforming growth factor-beta on low density lipoprotein (LDL) receptor-mediated cholesterol metabolism were evaluated in vascular smooth muscle cells and coincubation with pertussis toxin abrogated the effect of TGF- beta on LDL receptor expression, suggesting that a pertussi toxin-sensitive G-protein may be involved in the signal transduction pathway.
Oxidative alterations of cyclooxygenase during atherogenesis.
TL;DR: This review will include a discussion of how NO(x) species alter COX activity at the molecular level and how these modifications may contribute to altered eicosanoid output during atherosclerosis and lesion development.