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 Anupam
Agarwal, MD
agarwal@nersp.nerdc.ufl.edu
Dr. Agarwal is an Assistant Professor of Medicine our Division
at the University of Florida. He graduated from medical school in
India, in 1985 and completed his internal medicine residency and
a fellowship in nephrology from the Postgraduate Institute of Medical
Education and Research, Chandigarh, India. Prior to joining this
division in 1995, he received training in nephrology at the University
of Minnesota under the direction of Dr. Thomas Hostetter. During
his fellowship at the University of Minnesota, he spent two years
in the laboratory of Dr. Karl Nath working on adaptive mechanisms
in acute renal injury. He was awarded a Young Investigator Grant
from the National Kidney Foundation, and also received a NIH Clinical
Investigator Award to pursue additional training in cell and molecular
biology in the laboratory of Dr. Harry S. Nick, at the University
of Florida. He has been an Assistant Professor of Medicine in the
Division of Nephrology, Hypertension and Transplantation since January
1997.
Research Interest
My principal interests in clinical nephrology include acute renal
failure, specifically in the intensive care unit setting, toxic
nephropathies, fluid and electrolyte disorders, glomerular disorders,
progression of renal disease, and diabetic nephropathy. My long
term goals are to pursue a career in academic nephrology with the
primary focus being on basic research, teaching and patient care.
My goal is to apply knowledge gained from bench research to the
bedside, enabling research to be a significant contributor to advancement
in clinical medicine.
The area of my present research is in cell and molecular biology.
My specific aim is to study renal pathophysiology using molecular
biology techniques. Currently, I am exploring the molecular mechanisms
involved in the regulation of a redox sensitive gene, heme oxygenase,
that is induced in the kidney, in response to oxidant injury. One
of the products of the heme oxygenase catalyzed reaction is carbon
monoxide, which like nitric oxide, has received considerable attention
as a signaling molecule. Induction of heme oxygenase is considered
to be a generalized adaptive and beneficial response to oxidative
stress in cells and tissues. Our previous observations demonstrate
that such a response also occurs in acute renal injury and serves
a protective function in the models we have studied (eg. cisplatin-induced
toxic nephropathy, acute renal transplant rejection). Another area
of interest involves oxidative injury in renal tubular epithelial
cells exposed to oxidized low density lipoprotein (LDL).
My laboratory is currently studying regulation of the heme oxygenase
gene in human renal proximal tubular cells. We are performing studies
to identify regulatory elements in the promoter region of the human
heme oxygenase gene responsive to oxidant stimuli. Studies are also
being performed to evaluate the functional significance of heme
oxygenase in cell injury and transgenic animal models.
Our studies include state-of-the-art techniques such as polymerase
chain reaction (PCR), long range PCR, recombinant DNA methods, promoter
deletion analysis, transfections (transient and stable), chromatin
structure analysis by DNase I hypersensitive analysis and in vivo
footprinting, to study DNA-protein interactions to identify possible
transcription factors. These studies would help us to identify regions
of the gene that regulate its expression and may help to design
molecular based therapeutic approaches in renal injury, wherein
this gene is upregulated.
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