The purpose of Core B - Analytic and Synthetic Chemistry is to carry out two critical functions for each of theprojects. These functions require special scienitific expertise and expensive equipment so establishing acore provides an effective and efficient mechanism to accomplish essential features of the proposal. Theanalytic component of the core will serve all 4 projects and will use mass spectroscopy to identify andcharacterize oxidized phospholipid species derived from PC and PS. The core is well equipped with state-of-the-art mass spectroscopy equipment. The synthetic chemistry component of the core will synthesize welldefined, unique oxidized phospholipid species to be used by all projects to precisely define the role ofspecific receptors, transporters, ligands and enzymes in mediating cellular responses to oxidized lipids. Weare combining two functions (analytic and synthetic) into a single core because the two activities are quiteinterdependent. The synthetic lipids generated will be analyzed and their structures verified by the analyticcomponent with mass spectroscopy and the oxidized phospholipid species identified in the analyticcomponent will then be synthesized by the synthesis component.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
1P01HL087018-01A1
Application #
7337251
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
2007-07-01
Project End
2012-04-30
Budget Start
2007-07-01
Budget End
2008-04-30
Support Year
1
Fiscal Year
2007
Total Cost
$350,969
Indirect Cost
Name
Cleveland Clinic Lerner
Department
Type
DUNS #
135781701
City
Cleveland
State
OH
Country
United States
Zip Code
44195
Silverstein, Roy L (2018) Oxidized Lipid Uptake by Scavenger Receptor CD36 (Cluster of Differentiation 36) Modulates Endothelial Surface Properties and May Contribute to Atherogenesis. Arterioscler Thromb Vasc Biol 38:4-5
Chen, Yiliang; Huang, Wenxin; Yang, Moua et al. (2017) Cardiotonic Steroids Stimulate Macrophage Inflammatory Responses Through a Pathway Involving CD36, TLR4, and Na/K-ATPase. Arterioscler Thromb Vasc Biol 37:1462-1469
Silverstein, Roy L (2017) Linking Metabolic Dysfunction to Atherosclerosis Via Activation of Macrophage CD36 Gene Transcription by Retinol Binding Protein-4. Circulation 135:1355-1356
Ramakrishnan, Devi Prasadh; Hajj-Ali, Rula A; Chen, Yiliang et al. (2016) Extracellular Vesicles Activate a CD36-Dependent Signaling Pathway to Inhibit Microvascular Endothelial Cell Migration and Tube Formation. Arterioscler Thromb Vasc Biol 36:534-44
Gupta, Nilaksh; Li, Wei; McIntyre, Thomas M (2015) Deubiquitinases Modulate Platelet Proteome Ubiquitination, Aggregation, and Thrombosis. Arterioscler Thromb Vasc Biol 35:2657-66
Chadwick, Alexandra C; Holme, Rebecca L; Chen, Yiliang et al. (2015) Acrolein impairs the cholesterol transport functions of high density lipoproteins. PLoS One 10:e0123138
Chen, Yiliang; Kennedy, David J; Ramakrishnan, Devi Prasadh et al. (2015) Oxidized LDL-bound CD36 recruits an Na?/K?-ATPase-Lyn complex in macrophages that promotes atherosclerosis. Sci Signal 8:ra91
Latchoumycandane, Calivarathan; Nagy, Laura E; McIntyre, Thomas M (2014) Chronic ethanol ingestion induces oxidative kidney injury through taurine-inhibitable inflammation. Free Radic Biol Med 69:403-16
Gupta, Nilaksh; Li, Wei; Willard, Belinda et al. (2014) Proteasome proteolysis supports stimulated platelet function and thrombosis. Arterioscler Thromb Vasc Biol 34:160-8
Srikanthan, S; Li, W; Silverstein, R L et al. (2014) Exosome poly-ubiquitin inhibits platelet activation, downregulates CD36 and inhibits pro-atherothombotic cellular functions. J Thromb Haemost 12:1906-17

Showing the most recent 10 out of 88 publications