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Arthi Kanthasamy

Arthi Kanthasamy
Arthi Kanthasamy

Ph.D.

Associate Professor
Biomedical Sciences
(515) 294-7238
2024 Vet Med
Expertise / Research Area

  • Oxidative stress
  • Parkinson’s Disease
  • Cerebral Ischemia
  • Neuroinflammatory events
  • Dopamine

 

Dr. Arthi Kanthasamy’s research focuses on the cellular and molecular mechanisms underlying neurodegenerative processes associated with cerebral ischemia, drugs of abuse, and Parkinsons’s disease.  Brain ischemic damage results from occlusion of cerebral arteries that supply brain cells.  If the blockade is not reversed within a defined short period, it leads to induction of cell death within the region that is supplied by the affected vessels.  The goals of her lab are two fold: 1)  To elucidate the role of novel PKC isoform cell signaling events in apoptotic death of striatal neurons; 2)  To evaluate the influence of excessive dopamine in striatal neuronal oxidative damage during cerebral ischemia. 

 

Parkinson’s disease is a progressive age related neurodegenerative disease characterized by pronounced loss of the dopaminergic neurons in the substantia nigra pars compacta (SNc).  To identify the cellular mechanisms underlying selective loss of dopaminergic neurons in PD, Dr. Kanthasamy has collaborated to developed a unique in vitro dopaminergic cell culture model to study the importance of autophagic degradative machinery in dopaminergic neuronal loss.  Her recent studies indicate a functional link between the ubiquitin proteasomal system and autophagy.  A dynamic balance between the two degradative machineries is essential for the normal functioning of the cell.  Therefore, she is interested in examining the functional interaction between the two protein degradation systems in a chemical-induced model of Parkinson’s disease.  The dopaminergic toxicant methamphetamine is used as a key inducer of autophagy and apoptosis.  She is studying the signal transduction mechanisms associated with cross talk between autophagy and apoptosis in mediating neuronal degeneration. Genetic, proteomic, biochemical, cell biological,  pharmacological, neurochemical, behavioral and electron microscopic (TEM) approaches.  Currently, Dr. Kanthasamy is collaborating with Dr. Syed Ali at the National Center for Toxicological Research, United States Food and Drug Administration at Arkansas.

 

Another major focus of her research is to understand the role of neuroinflammatory events in PD induced dopaminergic neuronal loss.  She is studying the functional interaction between activated microglia and dopaminergic neurodegeneration in experimental models of Parkinson’s disease.  Understanding the cellular events underlying microglia-mediated neurodegeneration may be critical in developing novel therapeutic strategies that limit the progressive loss of dopaminergic neurons in PD related chronic neurodegenerative disease

 

 

 

 

Selected Publications

  1. Kaul, S., et al. "Tyrosine phosphorylation regulates the proteolytic activation of protein kinase Cdelta in dopaminergic neuronal cells." J Biol Chem. 280.31 (2005): 28721-30.
  2. Kanthasamy, A. G., et al. "A novel peptide inhibitor targeted to caspase-3 cleavage site of a proapoptotic kinase protein kinase C delta (PKCdelta) protects against dopaminergic neuronal degeneration in Parkinson's disease models." Free Radic.Biol Med. 41.10 (2006): 1578-89.
  3. Zhang, D., et al. "Neuroprotective effect of protein kinase C delta inhibitor rottlerin in cell culture and animal models of Parkinson's disease." J Pharmacol Exp Ther. 322.3 (2007): 913-22.
  4. Zhang, D., et al. "Protein kinase C delta negatively regulates tyrosine hydroxylase activity and dopamine synthesis by enhancing protein phosphatase-2A activity in dopaminergic neurons." J Neurosci. 27.20 (2007): 5349-62.
  5. Sun, F., et al. "Proteasome inhibitor-induced apoptosis is mediated by positive feedback amplification of PKCdelta proteolytic activation and mitochondrial translocation." J Cell Mol.Med. 12.6A (2008): 2467-81.
  6. Kanthasamy, A. G., et al. "Environmental neurotoxin dieldrin induces apoptosis via caspase-3-dependent proteolytic activation of protein kinase C delta (PKCdelta): Implications for neurodegeneration in Parkinson's disease." Mol.Brain. 1.1 (2008): 12.
  7. Sun, F., et al. "Mitochondrial accumulation of polyubiquitinated proteins and differential regulation of apoptosis by polyubiquitination sites Lys-48 and -63." J Cell Mol.Med. (2009).


Honors & Awards

In 2009, Dr. Kanthasamy received funding from the NINDS’ “New Investigator Award” program. She will receive a total of $1.28 million for her work in researching brain inflammatory mechanisms of Parkinson ’s disease models.   

Awards:

National Institutes of Health, NINDS “New Investigator Award,” 2009

Young Scientist Award, Association of Scientists of Indian Origin in America -Neuroscience Division, 2006

Outstanding Research Presentation Award at Purdue University Neuroscience (PUN) Retreat, 1999

Summer fellowship from Parkinson’s Disease Foundation for the project titled, “Mechanisms of neuroprotective effect of strychnine-insensitive glycine site antagonists in an experimental Parkinson’s model: Effects on cellular bioenergtics and MPP+ bio-disposition, 1996

Summer fellowship from Parkinson’s Disease Foundation for the project titled, “Biochemical, behavioral and histological characterization of strychnine-insensitive glycine site antagonists in an experimental Parkinson’s model,” 1995