In This Section

Prasun K. Datta, PhD

Assistant Professor, Neuroscience
Assistant Professor, Neurovirology

Prasun Datta
Contact Information

Contact Information

Phone

215-707-4938

Fax

215-707-4888

Email

dattapk@temple.edu
About Me

Research Interests

Our laboratory's current research efforts focus on studying novel mechanisms involved in HIV-1 biogenesis and survival in latent CNS reservoirs, and the effects of HIV-1 induced neuroinflammatory cytokines and exosomes on astrocyte glutamate transporter, EAAT2 and neurodegeneration, respectively. In addition, we are also interested in assessing the impact of drugs of abuse such as opiate and cocaine on HIV-1 biogenesis and astrocyte EAAT2 gene regulation. The projects are:

A. Epigenetics of EAAT2 regulation:

The Excitatory amino acid transporter-2 (EAAT2) is the major glutamate transporter expressed predominantly by astrocytes in the brain. Glutamate transport is central to neurotransmitter functions in the brain. Dysregulation of glutamate transport induces neurotoxicity associated with numerous pathological processes, including HIV-1-associated dementia, Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and stroke/ischemia. Our laboratory is interested in understanding the role of epigenetic mechanisms such as DNA methylation, microRNAs and chromatin modification in the regulation of EAAT2 expression specifically in the context of NeuroAIDS. Our long term goal is to identifying therapeutic approaches that are capable of modulating EAAT2 expression that could potentially inhibit, ameliorate, or prevent various neurodegenerative diseases.

B. Cross-talk between HIV-1 and glucose metabolism:

Our recent work is also focused on the elucidation of how HIV-1 hijacks the macrophage glucose metabolism pathway via the Vpr-HIF-1 alpha axis to create an environment that is not only advantageous for viral replication and biogenesis, but also for long-term survival of infected macrophages. These studies are aimed to help formulate novel therapeutic approaches that targets glucose metabolism to mitigate HIV replication and survival in macrophages.

C. HIV-1 infected cell derived Exosomes and Neurodegeneration:

Our newest line of research focuses on exosomes (extracellular membranous vesicles) specifically those produced as a consequence of reactivation of HIV-1 in latent CNS reservoirs such as macrophages and microglia. Our current efforts are focused on the characterization of exosomal nucleic acid cargo using microarray technology and the protein cargo using proteomics approach. Using a global proteomic approach we are also deciphering the mechanism of exosome-mediated neurodegeneration.

D. Complement regulation in context of NeuroAIDS:

Our laboratory is also interested in elucidating the regulation and role of the Complement system in the context of NeuroAIDS. The complement system is one of the key players in the innate immune defense against pathogens. Complement activation in excess can promote inflammation and tissue damage. Numerous studies in the last one and half decade have demonstrated that the complement system is activated by HIV and the system plays a significant role in HIV pathogenesis.

Education, Training & Credentials

Educational Background

  • Postdoctoral Fellowship, Department of Pharmacology and Molecular Biology, Chicago Medical School
  • PhD, University of Calcutta

Memberships

  • American Association of Advancement of Science
  • International Society of Neurovirology
  • Society on NeuroImmune Pharmacology
  • International Complement Society
Publications

PubMed Publications

View PubMed Publications

Additional Publications

Book Chapters:

Datta PK and Lianos EA. Role of Eicosanoids in Glomerular, Tubular and Vascular injury. In: Massry, SG, and Glassock, RJ. (Eds), Textbook of Nephrology, 4th Edition, 2000, Chapter 37, Part 4, William & Wilkins, Baltimore, MD.

Datta, PK and Lianos, EA. 2002. Regulation and role of Heme oxygenase-1 in glomerulonephritis. In: Heme Oxygenase in Biology and Medicine, Abraham, NG, Alam, J and Nath, KA. (Eds), Springer, pp 251-258.