Tanusree Sen, PhD

Research Assistant Professor

Tanusree Sen




Tanusree Sen, PhD, joined the University of Pittsburgh Department of Neurological Surgery in March of 2017 as a research assistant professor.

As part of her PhD training, she developed expertise in the area of oxidative stress-mediated cellular dysfunctions and brain aging. In 2007 after her graduation, she joined the research group of David Sidransky, MD, at Johns Hopkins University’s Division of Head and Neck Cancer. In Dr. Sidransky lab, Dr. Sen worked on multiple projects unraveling the molecular pathways and mechanism involving in different cancer including cigarette smoking-induced bladder cancer. Her work studied the mechanism involved p53 isoform, p63 for cell death and chemoresistance and she discovered novel mechanisms which were shown to play a key role in cell death associated with several different cancer. In a separate project of age-related macular degeneration, she discovered the key role of lens structural protein CRYBA1 in anoikis and autophagy process in mouse retinal astrocytes and retinal pigmented epithelial cells.

In 2012, Dr. Sen joined Augusta University as a postdoctoral fellow and extended her expertise of cellular-molecular biology in the field of immunology, autoimmunity and traumatic brain injury and discovered molecular mechanism regulating neuronal death and memory function after traumatic brain injury.

In 2015, Dr. Sen started working as a research assistant professor at the University of Georgia and worked on the mechanism of diet-induced vagal nerve injury specifically in the context of the gut-microbiota-inflammation-brain axis. At this time she discovered how different diet may contribute to gut microbial dysbiosis, inflammation and subsequently damage to the vagal nerve. Dr. Sen has published 33 papers in refereed journals with total citations have exceeded 2500.

Specialized Areas of Interest

Studying the influence of oncogenic transcription factors on the TBI-pathology; regulation of immune response and its influence on cognitive dysfunction following TBI; studying the role of resident microbial cells on TBI-pathology

Professional Organization Membership

Society for Neuroscience

Education & Training

BSc, Chemistry, Calcutta University, India 1998 
MSc, Biochemistry, Calcutta University, India, 2000 
PhD, Aging, Mitochondrial function, membrane potential, University of Calcutta, 2006 
Fellowship, oncogenic activation, cell death and proliferation, Johns Hopkins, 2010

Honors & Awards

  • Awarded Junior Research Fellowship in the Life-Sciences category, University Grants Commission (UGC), India, 2000
  • Awarded Lectureship and Research Fellowship by the Council for Scientific and Industrial Research, India, 2001
  • Awarded Senior Research Fellowship by the Council for Scientific and Industrial Research, India, 2003
  • Best Oral Presentation Award at International Symposium on Free Radical Research, India, 2006
  • Finalist in Young Scientist Award Lecture, Society for Free Radical Research, India, 2006

Selected Publications

Sen T, Gupta R, Kaiser H, Sen N. Activation of PERK Elicits Memory Impairment through Inactivation of CREB and Downregulation of PSD95 After Traumatic Brain Injury. J Neurosci 37(24):5900-5911, 2017.

Vaughn AC, Cooper EM, DiLorenzo PM, O'Loughlin LJ, Konkel ME, Peters JH, Hajnal A, Sen T, Lee SH, de La Serre CB, Czaja K. Energy-dense diet triggers changes in gut microbiota, reorganization of gut‑brain vagal communication and increases body fat accumulation. Acta Neurobiol Exp (Wars) 77(1):18-30, 2017.

Sen T, Cawthon CR, Ihde BT, Hajnal A, DiLorenzo PM, de La Serre CB, Czaja K. Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity. Physiol Behav 173:305-317, 2017.

Sen T, Sen, N. Isoflurane-induced inactivation of CREB through histone deacetylase 4 is responsible for cognitive impairment in developing brain. Neurobiol Dis 96:12-21, 2016

Sen T, Sen N. Treatment with an activator of hypoxia-inducible factor 1, DMOG provides neuroprotection after traumatic brain injury. Neuropharmacology 107:79-88, 2016.

Mir S, Sen T, Sen N. Cytokine-induced GAPDH sulfhydration effects PSD95 degradation and memory. Mol Cell 56:786, 2014.

Sen T, Sen N, Noordhuis MG, Ravi R. Wu TC, Ha PK, Sidransky D, Hoque MO. OGDHL is a modifier of AKT-dependent signaling and NF-kB function. PLoS One 7(11):e48770, 2012.

Sen N, Paul BD, Gadalla MM, Mustafa AK, Sen T, Kim S, Snyder SH. Hydrogen sulfide-linked sulfhydration of NF-kB mediates its anti-apoptotic actions. Mol Cell 45(1),13-24, 2012

Sen T. Sen N, Huang Y, Sinha D, Ratovitski E, Sidransky D. Tumor protein p63/nuclear factor kappa-B axis in regulation of cell death. J Biol Chem 286(50): 43204-13, 2011.

Sen T, Sen N, Brait M, Begum S, Chatterjee A, Hoque M, Ratovitski E, Sidransky D. ΔNp63alpha confers tumor cell resistance to cisplatin treatment through the transcriptional regulation of AKT. Cancer Res 71(3):1167-76, 2011.

Sen T, Chang X, Sidransky D, Chatterjee A. Regulation of ΔNp63α by NF-κΒ. Cell Cycle 9(24):4841-7, 2010.

Huang Y, Sen T, Nagpal J, Upadhyay S, Trink B, Ratovitski E, Sidransky D. Equal contributory first author. ATM kinase is a master switch for the ΔNp63 alpha phosphorylation/degradation in human head and neck squamous cell carcinoma cells upon DNA damage. Cell Cycle 7(18), 2846-55, 2008.

A complete list of Dr. Sen's publications can be reviewed through the National Library of Medicine's publication database.

Research Activities

The activation of an oncogenic transcription factor in the peripheral tissues have been well studied; however, the influence of these factors on the brain function and neurological disorders have not been studied to that extent. Dr. Sen would like to elucidate the function of these transcription factors on several pathological outcomes of TBI, which is characterized by an induction of cell death, edema, inflammation and cognitive dysfunction.

Dr. Sen’s preliminary data indicate that a transcription factor, p63, which is a family member of the tumor suppressor, contributes to the pathological outcomes of TBI in several layers. In addition, Dr. Sen is in a process to understand the cellular and molecular mechanism of how p63 regulates the oxidative/ER stress, alteration in mitochondrial structure and function and cognitive impairment.

In addition, Dr. Sen have been working to understand whether the immune cells from the peripheral tissues contributes to brain immunological response following TBI. In general, the peripheral immune cells cannot enter unto the brain because they can not pass through the blood-brain barrier. However, in TBI patients the existence of peripheral immune cells has been identified, but their role in the pathogenicity has not been studied well.  The major objective of this project is to understand how these cells enter into the brain and how/whether they function independently or in association with the residential immune cells in the brain.

In the last few years, Dr. Sen has studied the functional aspects of transcription factors such CREB and HIF1 and their contribution to release of a neurotransmitter, such as BDNF in the brain and neurogenesis and angiogenesis processes following TBI. Dr. Sen would like to combine her experience of studying oncogenic transcription factors and function of immunological cells with the expertise of studying several aspects of TBI-pathology to accomplish the goals and objectives of current projects.