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.
- Oxidation of plasmalogens, low-density lipoprotein and RAW 264.7 cells by photoactivatable atomic oxygen precursors.
Bourdillon MT, Ford DA, et al. Photochem Photobiol. (2014), in press.
- Inhibiting monoacylglycerol acyltransferase 1 ameliorates hepatic metabolic abnormalities, but not inflammation and injury in mice.
Soufi N, Hall AM, et al. J Biol Chem. (2014) Sept 11 [Epub ahead of print].
- Lipidomic analyses of female mice lacking hepatic lipase and endothelial lipase indicate selective modulation of plasma lipid species.
Yang Y, Kuwano T, et al. Lipids. (2014) 49(6):505-515.
- Elaidic acid increases hepatic lipogenesis by mediating sterol regulatory element binding protein-1c activity in HuH-7 cells.
Shao F, Ford DA. Lipids. (2014) 49(5):403-413.
- Alpha-chlorofatty acid accumulates in activated monocytes and causes apoptosis through reactive oxygen species production and endoplasmic reticulum stress.
Wang WY, Albert CJ, et al. Arterioscler Thromb Vasc Biol (2014) 34(3):526-532.
- Dietary omega-3 polyunsaturated fatty acids alter the fatty acid composition of hepatic and plasma bioactive lipids in C57BL/6 mice: A lipidomic approach.
Balogun KA, Albert CJ, et al. PLoS One. (2013) 8(11):e82399.
- LXRs regulate ER stress and inflammation through dynamic modulation of membrane phospholipid composition.
Rong X, Albert CJ, et al. Cell Metab. (2013) 18(5):685-97.
- 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) 2:e125.
- Approaches for the analysis of chlorinated lipids.
Wang W, Albert CJ, and Ford DA. Anal Biochem. (2013) 443(2):148-52.
- 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) 59(4):731-7.
- 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.