David A. Ford, Ph.D.
Biochemical mechanisms responsible for the pathophysiological sequelae of cardiovascular diseases, including ischemic heart disease and atherosclerosis.
Office: DRC, Room 325
Voice: (314) 977-9264
Ph.D., 1985, University of Missouri-Columbia
We are interested in biochemical mechanisms responsible for the pathophysiological sequelae of cardiovascular diseases including ischemic heart disease and atherosclerosis. Areas of research focus on enzymic and free radical targeting of membrane phospholipids, alterations in lipid metabolism, and alterations in signaling pathways as mechanisms involved in cardiovascular diseases. We combine our expertise using physiological models of disease coupled with expertise in mass spectrometry and bioorganic techniques to reveal new mechanistic insights into cardiovascular disease.
- LXRs regulate ER stress and inflammation through dynamic modulation of membrane phospholipid composition.
Rong X, Albert CJ, et al. Cell Metab. (2013), in press.
- Long-term expression of apolipoprotein B mRNA-specific hammerhead ribozymes via scAAV8.2 vector inhibit atherosclerosis in mice.
Nischal H, Sun H, et al. Mol Ther Nucleic Acids. (2013) Oct 1 [Eppub ahead of print].
- Approaches for the analysis of chlorinated lipids.
Wang W, Albert CJ, and Ford DA. Anal Biochem. (2013) Sept 19 [Epub ahead of print].
- Differential regulation of ABCA1 and macrophage cholesterol efflux by elaidic and oleic acids.
Shao F and Ford DA. Lipids. (2013) 48(8):757-67.
- Hydrolysis products generated by lipoprotein lipase and endothelial lipase differentially impact THP-1 macrophage cell signaling pathways.
Essaji Y, Yang Y, et al. Lipids. (2013) 48(8):769-78.
- Impaired liver regeneration in Ldlr -/- mice is associated with an altered hepatic profile of cytokines, growth factors, and lipids.
Pauta M, Rotllan N, et al. J Hepatol. (2013) S0168-8278(13):00358-9.
- Absence of myocardial calcium-independent phospholipase A2γ results in impaired PGE2 production and decreased survival in mice with acute Trypanosoma cruzi infection.
Sharma J, Eickhoff CS, et al. Infect Immun. (2013) 81(7):2278-87.
- Acyl-CoA synthetase 1 is induced by gram-negative bacteria and lipopolysaccharide and is required for phospholipid turnover in stimulated macrophages.
Rubinow KB, Wall VZ, et al. J Biol Chem. (2013) 288(14):9957-70.
- Obesity-related alterations in cardiac lipid profile and nondipping blood pressure pattern during transition to diastolic dysfunction in male db/db mice.
Demarco VG, Ford DA, et al. Endocrinology. (2013) 154(1):159-71.
- Cholesterol efflux analyses using stable isotopes and mass spectrometry.
Brown RJ, Shao F, et al. Anal Biochem. (2012) 433(1):56-64.
- Dietary trans-fatty acid induced NASH is normalized fFollowing loss of trans-fatty acids from hepatic lipid pools.
Neuschwander-Tetri BA, Ford DA, et al. Lipids. (2012) 47(10):941-50.
- miR-33 controls the expression of biliary transporters, and mediates statin- and diet-induced hepatotoxicity.
Allen RM, Marquart TJ, et al. EMBO Mol Med. (2012) 4(9):882-95.
- Strategies for the analyses of chlorinated lipids in biological systems.
Wacker BK, Albert CJ, et al. Free Radic Biol Med. (2012) 59:92-9.
- MALDI mass spectrometric imaging of cardiac tissue following myocardial infarction in a rat coronary artery ligation model.
Menger RF, Stutts WL, et al. Anal Chem. (2012) 84(2):1117-25.