Tanusree Sen, PhD

Research Assistant Professor


Tanusree Sen

Contact

412-647-3685

Biography

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 35 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; tauopathy 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, Brain Aging, University of Calcutta, 2006 
Fellow, Head and Neck Cancer, Johns Hopkins, 2010
Fellow, Cancer Immunology and Neuroscience, Augusta University, 2014

Honors & Awards

  • Best Oral Presentation Award, International Symposium on Free Radical Research, India, 2006
  • Finalist, 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

Dr. Sen has been continuing her effort to identify novel function of transcription factor p63 in cognitive function and TBI pathology. Her preliminary data indicate that a transcription factor, p63 contributes to the pathological outcomes of TBI in several layers including regulation of oxidative/ER stress, alteration in mitochondrial structure and function and cognitive impairment. She is currently working on understating the role of p63 in induction of cell death, edema, and neurogenesis.

In another effort, Dr. Sen recently identified that mitochondrial dysfunction due to decreased mitochondrial mass contributes to cognitive dysfunction following TBI. As a part of the mechanism, she showed that cyclin D1 regulates the transcriptional activity of a key factor which critically regulates mitochondrial mass following TBI.

In addition, her recent studies have shown that an increase in acetylation of Tau induced by nitric oxide contributes to tauopathy. To elucidate the molecular mechanism, Dr. Sen found that an increase in nitrosylation of a rate-limiting glycolytic enzyme GAPDH facilitates Tau acetylation and tauopathy. She is in the process of understanding whether tau acetylation contributes to tauopathy following TBI.

Furthermore, she has also been working on immune cells modulation in brain following TBI. Dr. Sen is continuing her effort to identify novel therapeutic strategies to attenuate the inflammatory pathways that contributes to TBI pathology. She is combining 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.