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Madhulika Dixit

madhulika-dixit
Associate Professor
Ph.D, Indian Institute of Technology Bombay
M.Sc, University of Mumbai
Office: BT 402
Tel: +91-44-2257-4131
Email: mdixit@iitm·ac·in
Lab: BT 415 (Website)

Research Interests

The primary objective of my research team is to elucidate molecular and cellular mechanisms of normal and aberrant function of blood vessels under physiological and patho-physiological conditions respectively. The key areas we focus on are endothelial dysfunction, atherosclerosis and edema. In order to obtain a holistic picture on these issues we would subscribe to the following approaches:

  • High through put screening for identification of changes in gene expression from clinical samples.
  • In vitro tissue culture experiments to identify signaling intermediates altered under pathological settings. For this we would employ primary cultures of vascular smooth muscle cells (VSMCs), and human umbilical vein endothelial cells (HUVECs).
  • Validation of in vitro data through in vivo animal experiments.
  • Use of viral vector based gene delivery systems to rectify the faulty functioning of the signaling intermediates.

Publications

  • Kodigre, P., Dixit, M., and Rao, K.K. “ScoC and SinR negatively regulate epr by corepression in Bacillus Subtilis.” Journal of Bacteriology, 2006; 188 (17): 6425-6428.
  • Dixit, M., Loot, A.E., Mohamed, A., Fisslthaler, B., Boulanger, C.M., Ceacareanu, B., Hassid, A., Busse, R., and Fleming, I. “ Gab1, SHP2 and Protein kinase A are crucial for the activation of the endothelial nitric oxide synthase by fluid shear stress.” Circulation Research, 2005; 97 (12):1236 -1244.
  • Fleming, I., Fisslthaler, B., Dixit, M., and Busse, R. “Role of PECAM-1 in the shear stress-induced activation of Akt and the endothelial nitric oxide synthase (eNOS) in endothelial cells.” Journal of Cell Sciences, 2005; 118 (18): 4103-4111.
  • Zhuang, D., Ceacareanu, AC., Lin, Y., Ceacareanu, B., Dixit, M., Chapmann, K.E., Waters, C.M., Rao, G.N., and Hassid, A. “Nitric oxide attenuates insulin- or IGF-1-stimulated aortic smooth muscle cell motility by decreasing H2O2 levels: essentialrole of cGMP.” American Journal of Physiology, Heart and Circulatory Physiology, 2004; 286: H2103-H2112.
  • Dixit, M., Ceacareanu, B., Zuang, D., and Hassid, A. “Nitric Oxide-Induced Motility of Aortic Smooth Muscle cells: Requirement for Gab1 and Gab1-SHP2 association.” Ultra rapid communications, Circulation Research, 2003; doi: 10.1161/01.RES.0000100391. 98425.BB.
  • Chang, Y., Ceacareanu, B., Dixit, M., Nair, S and Hassid, A. 2002. “Nitric Oxide- Induced Motility in Aortic Smooth Muscle cells, Role of Protein Tyrosine Phosphatase SHP-2 and GTP Binding Protein Rho.” Circulation Research, 2002; 91, 390-397.
  • Dixit, M., Murudkar, C. S. and Rao, K.K. 2002.” epr is Transcribed from a D Promoter and is Involved in Swarming of Bacillus subtilis.” Journal of Bacteriology, 2002; 184 (2): 596-599.
  • Dixit, M., Bess, E., Fisslthaler, B., Hartel, F.V., Noll, T., Busses., and Fleming,I. Shear stress-included activation of the AMP-activated protein kinase regulates Fox0la and angiopoietin-2 in endhothelial cells.” Cardiovascular Research, 2007; Manuscript in press.

Honours and Awards

  • IIT Madras Institute Research and Development Award (IRDA) 2014
  • IIT Madras Young Faculty Recognition Award (YFRA) 2013 for excellence in teaching
  • Senior Innovative Young Biotechnologist Award (Senior IYBA) 2011 by the Department of Biotechnology, Ministry of Science and Technology, Govt. of India.
  • Innovative Young Biotechnologist Award (IYBA) 2006 by the Department of Biotechnology, Ministry of Science and Technology, Govt. of India.