Dr. Rekha Kar's research is aimed at understanding the mechanisms that predispose diabetic patients to cardiovascular diseases. In particular, she is interested in elucidating the role of a nitric oxide-producing enzyme in modulating the susceptibility to cardiovascular dysfunction seen in diabetes using animal models of obesity and insulin resistance.
Diabetes is associated with increased oxidative stress, which causes cardiomyocyte death leading to defects in the myocardium and subsequent cardiac dysfunction. Nitric Oxide (NO) produced by the nitric oxide synthases (NOS) scavenges superoxide, which could potentially reduce overall oxidative stress. One of the potential sequelae of increased oxidative stress during diabetes could result from reduced NO bioavailability observed in diabetic patients, likely due to depletion of the substrate L-Arginine (L-Arg) and/or oxidation of the cofactor tetrahydrobiopterin (H4B).
Deletion of neuronal NOS (nNOS) in mice led to increased oxidative stress in heart, suggesting a critical role of this isoform of NOS in modulating oxidative stress. Her research showed that brief exposure to hydrogen peroxide (H2O2) induces phosphorylation of nNOS, whereas prolonged exposure reduces nNOS expression in cardiomyocytes. She is interested in determining the mechanisms of oxidative stress-induced regulation of nNOS function and the role of nNOS in regulating diabetic cardiomyopathy.
Dr. Kar will teach:
- CIRC 5003 Language of Medicine
- CSBL 5022 Inter-professional Anatomy
She will also direct the Summer Anatomy workshop held in June each year and possibly have future teaching activities in CSBL 5032 Dental Histology in the Fall of 2016.
Kar R, Kellogg DL 3rd, Roman LJ. (2015) Oxidative stress induces phosphorylation of neuronal NOS in cardiomyocytes through AMP-activated protein kinase (AMPK). Biochem Biophys Res Commun. 2015 Apr 10;459(3):393-7.
Riquelme MA, Burra S, Kar R, Lampe PD, Jiang JX. (2015) Mitogen-activated Protein Kinase (MAPK) Activated by Prostaglandin E2 Phosphorylates Connexin 43 and Closes Osteocytic Hemichannels in Response to Continuous Flow Shear Stress. J Biol Chem. 2015 Nov 20;290(47):28321-8.
Batra N, Riquelme MA, Burra S, Kar R, Gu S, Jiang JX. (2014) Direct regulation of osteocytic connexin 43 hemichannels through AKT kinase activated by mechanical stimulation. J Biol Chem. 2014 Apr 11;289(15):10582-91.
Kar R, Riquelme MA, Werner S, Jiang JX. (2013) Connexin 43 channels protect osteocytes against oxidative stress-induced cell death. J Bone Miner Res. 2013 Jul;28(7):1611-21.
Kar R, Batra N, Riquelme MA, Jiang JX. (2012) Biological role of connexin intercellular channels and hemichannels. Arch Biochem Biophys. 2012 Aug 1;524(1):2-15.