1. Lipoprotein Labeling by Alexa Fluor 2. Lipoprotein Labeling by DiI or DiO 3. LDL Oxidation 4. oxLDL Antibody Isolation by Affinity Chromatography 5. Immune Complex Formation 6. Lipoprotein Deficient Serum (LPDS) Preparation 7. Confocal Microscopy of Non-adherent Cells (fixed or alive) 8. Gas Chromatography for Cholesterol Determination 9. COBRE Protocols
3R01HL079274-04S1, Principal Investigator: Hammad, Type: NIH/NHLBI (ARRA), Title: Sphingolipid Signaling Induced by LDL Immune Complexes
1 R01 HL079274-01A2, Principal Investigator: Hammad, Type: NIH/NHLBI, Title: Sphingolipid Signaling Induced by LDL Immune Complexes. The main goals of this proposal is to uncover mechanisms by which modified LDL immune complexes suppress apoptosis of foam cells, and reveal specific targets in the signaling pathway that can have therapeutic implications for blocking cytokine release and to prevent formation of vulnerable plaques.
P20 RR17677-01 Obeid (PI)
COBRE in Lipidomics and Pathobiology: to develop an interactive Center of Lipidomics and Pathobiology that will promote the growth and excellence of research at MUSC.
Project 11 S. Hammad (PI) 11/01/05-6/30/09
Sphingolipid Signaling Induced by LDL Immune Complexes
The main goal is to characterize the activated downstream sphingolipid signaling response of macrophages to modified LDL-containing immune complexes.
Scientist Development Grant S. Hammad (PI) 7/1/04-4/1/06 American Heart Association, National Center
Sphingolipid signaling response to modified low density lipoprotein-immune complexes in human macrophages. The main goals of this project is to uncover mechanisms by which modified LDL-containing immune complexes suppress apoptosis of foam cells, and reveal specific targets in the signaling pathway such as receptors and/or sphingolipids that can have therapeutic implications for blocking cytokine release and prevention of vulnerable atherosclerotic plaques.
University Research Committee Award S. Hammad (PI) 1/1/05-12/31/06 Medical University of South Carolina Sphingolipid signaling induced by LDL immune complexes. Dr. Hammad (PI) obtained this supplementary funding to cover salary support for a full time technician (Mr. Goodman). Mr. Goodman is working closely with the PI and participates in various aspects of the proposed experiments.
Research Grant Lyons (PI) 9/1/01-8/30/04 Juvenile Diabetes Foundation International (JDFI) Markers and Mechanisms for Pre-Eclampsia in Women with Type 1 Diabetes The goal of this project is to explore markers and mechanisms for pre-eclampsia, which is a common vascular disease in diabetic pregnant women. Type 1 diabetic pregnancies from three centers (South Carolina; Melbourne, Australia; Oslo Norway) were recruited for the study. Role: Co-Principal Investigator
R01 DK58283-02 Luttrell (PI) 6/01/01-05/31/05 NIH/NIDDK Receptor "transactivation" in insulin signaling The major goals of this project were to determine the mechanisms and functional significance of cross talk between insulin receptors, heterotrimeric G proteins, and classical receptor tyrosine kinases. Role: Co-Investigator
P01 HL55782-07 Lopes-Virella (PI) 9/1/96- 8/31/06 NIH Program Project Grant Markers and Mechanisms of Vascular Disease in Diabetes (Research Project 2) The main goal of Project 2 is to compare the levels of soluble adhesion molecules and the levels and characteristics of LDL-immune complexes isolated from the sera of a type 2 diabetic cohort under intensive or standard glycemic control. Role: Co-Investigator
1R01-AG-16583 Obeid (PI) 9/1/01-8/31/05 NIH/NIA Mitochondrial Ceramide in Chemotherapy-induced Apoptosis The goals of this study are the following: 1) determine if generation of ceramide in mitochondria is sufficient to induce apoptosis, 2) determine the mechanism by which mitochondrial ceramide activates the apoptotic program, 3) determine if mitochondrial ceramide generation is necessary to activate apoptosis in response to chemotherapeutic agents, and 4) determine if modulating mitochondrial sphingolipids has therapeutic implications for cancer treatment. Role: Co-Investigator
M6311601MD10004 Obeid (PI) 6/1/02-7/31/04 Hollings Cancer Center/Department of Defense Translational Studies on the Role of Sphingosine Kinase in Lung Cancer The PI assembled a collaborative team to perform the following specific aims: 1) to demonstrate that sphingosine kinase will enhance tumor growth and angiogenesis, and 2) to demonstrate that inhibiting sphingosine kinase or decreasing sphingosine 1 phosphate levels will inhibit tumor growth. Role: Co-Investigator