Microbiology
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Faculty Detail
Name
GATTADAHALLI M ANANTHARAMAIAH
Campus Address
ZRB 517 Zip 0000
Phone
(205) 934-1884
E-mail
ananth@uab.edu
Other websites
Faculty Appointment(s)
Appointment Type
Department
Division
Rank
Primary
Med-Gerontology/Geriatrics/Palliative Care
Med-Gerontology/Geriatrics/Palliative Care
Professor Emeritus
Graduate Biomedical Sciences Affiliations
Biochemistry and Molecular Genetics Program
Biochemistry and Structural Biology
Cell, Molecular, & Developmental Biology
Medical Scientist Training Program
Microbiology
Neuroscience
Biographical Sketch
Dr. Anantharamaiah joined UAB in 1982 and is a Professor in the Department of Medicine. His research is supported by grants from NIH.
Research/Clinical Interest
Title
Apolipoproteins, Amphipathic Helices and Atherosclerosis
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).
