Dept. of Medicine
Division of Gerontology & Geriatric Medicine

Contact Information

Office Address: BDB 668
Phone: 205-934-1884
Websites: School of Medicine Faculty Profile


Bangalore University, India
BS, Physics, Chemistry and Math, 1967

Bangalore University, India
MS, Organic Chemistry, 1969

Bangalore University, India
PhD, Biologically Active Peptides, 1978

Post-Graduate Training:

Ohio State University, Columbus, OH

Postdoctoral Fellow, 1977-9

Research Interests:

Structure and function of plasma apolipoproteins. Apo-A1 structure and function. Apo-E structure and function. Structure of Apo-A-1 in alzheimer disease research. Research involves: Peptide synthesis, protein analysis. Biophysical, biochemical studies. Transgenic mouse technology. Molecular biology in vivo models of atherosclerosis.

Research Description:

Two mechanisms have been proposed for the progression of atherosclerosis: 1) the cholesterol theory, increased plasma cholesterol levels increased the risk for atherosclerosis 2) injury and endothelial surface perturbation is the major cause of atherosclerosis, which is inhibited by the presence of high levels of good cholesterol (HDL). It has been shown that both apo E (the protein component of very low-density lipoproteins (VLDL) and apolipoprotein A-I (the major protein component of HDL) are antiatherogenic, but by two distinctly different mechanisms. Using the common structural motif present for the lipid associating domains in apolipoproteins, the amphipathic helix, we have been able to design peptide mimics for 1) the rapid removal of atherogenic lipoproteins from circulation in vivo, and 2) inhibit atherosclerosis in atherosclerosis sensitive mice without changing plasma cholesterol profile. Using cell culture studies, we have determined that the peptides that reduce plasma cholesterol levels do so by enhancing their removal by the proteoglycan-mediated pathway. Cell culture studies have also shown that the peptides that inhibit atherosclerosis without altering plasma cholesterol levels do so by “removing the seeding molecules” from atherogenic lipoproteins. The laboratory is now in the process of producing transgenic mice expressing these two types of molecules and determining the exact mechanism(s) of atherosclerotic plaque formation and avenues to inhibit this (these) process(es).


DRC Membership Category:

Senior Scientist