Department of Cell Systems & Anatomy

CSA Faculty

 

Rekha Kar, Ph.D.

Lecturer II

 

University of Texas Health Science Center at San Antonio, 2008

 

DTL 1.275S
(210) 567-1567
Karr@uthscsa.edu

 

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.
My research is aimed at understanding the mechanisms that predispose diabetic patients to cardiovascular diseases. In particular, I am 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. We showed that brief exposure to hydrogen peroxide (H2O2) induces phosphorylation of nNOS, whereas prolonged exposure reduces nNOS expression in cardiomyocytes. I am interested in determining the mechanisms of oxidative stress-induced regulation of nNOS function and the role of nNOS in regulating diabetic cardiomyopathy.
Recent Publications:
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.

 

Representative Publications:
Kar R, Singha PK, Venkatachalam MA, Saikumar P. (2009) A novel role for MAP1 LC3 in nonautophagic cytoplasmic vacuolation death of cancer cells. Oncogene. 2009 Jul 16;28(28):2556-68.

 

Kar R, Mishra N, Singha PK, Venkatachalam MA, Saikumar P. (2010) Mitochondrial remodeling following fission inhibition by 15d-PGJ2 involves molecular changes in mitochondrial fusion protein OPA1. Biochem Biophys Res Commun. 2010 Sep 3;399(4):548-54.

 

Xia X, Kar R, Gluhak-Heinrich J, Yao W, Lane NE, Bonewald LF, Biswas SK, Lo WK, Jiang JX. (2010) Glucocorticoid-induced autophagy in osteocytes. J Bone Miner Res. 2010 Nov;25(11):2479-88.