Update Your ProfileAcademic Title:
Assistant Professor
Primary Appointment:
Anesthesiology
Location:
MSTF # 6-00
Phone (Primary):
(410) 706-0505
Fax:
(410) 328-5531
Education and Training
B. Pharm.: Jadavpur University, India
M. Tech. (Biotechnology): Jadavpur University, India
PhD: Indian Institute of Chemical Biology, Jadavpur University, India
Postdoctoral trainings: National Institutes of Health, Bethesda, MD and University of Maryland School of Medicine, Baltimore, MD
Research/Clinical Keywords
Traumatic brain injury, neurodegeneration, neuroinflammation, neuroprotection, aging, peroxisome, lysosome, lipid, autophagy
Highlighted Publications
Hegdekar N, Lipinski MM*, Sarkar C*. N-Acetyl-L-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice. Sci. Rep., 2021, Apr 29;11(1):9249. (*Corresponding author).
Sarkar C*, Sadhukhan T, Bagh MB, Appu AP, Chandra G, Mondal A, Saha A, Mukherjee AB*. Cln1-/- mutations Suppress Rab7-RILP Interaction and Impair Autophagy Contributing to Neuropathology in a Mouse Model of Infantile Neuronal Ceroid Lipofuscinosis. J Inherit Metab Dis. 2020 Sep;43(5):1082-1101. PMID: 32279353. (*Corresponding author).
Sarkar C, Jones JW, Hegdekar N, Thayer JA, Kumar A, Faden AI, Kane MA and Lipinski MM. PLA2G4A/cPLA2-mediated lysosomal membrane damage leads to inhibition of autophagy and neurodegeneration after brain trauma. Autophagy. 2020 Mar;16(3):466-485. PMID: 31238788.
Liu S, Li Y, Choi HMC, Sarkar C, Koh EY, Wu J# and Lipinski MM#. Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis. Cell Death & Disease. 2018; 9:476. PMID: 29686269
Awad O, Sarkar C, Panicker LM, Miller D, Zeng X, Sgambato JA, Lipinski MM, Feldman RA. Altered TFEB-mediated lysosomal biogenesis in Gaucher disease iPSCs-derived neuronal cells. Hum Mol Genet. 2015; 24(20):5775-88. PMID: 26220978.
Sarkar C., Zhao Z., Aungst S., Sabirzhanov B., Faden A. I. and Lipinski M. M. Impaired autophagy due to lysosomal dysfunction is associated with neuronal cell death after TBI. Autophagy 2014;10(12):2208-22. PMID: 25484084.
Sarkar C., Chandra, G., Zhang, Z., Peng S., Liu A. and Mukherjee A. B. Neuroprotection and lifespan extension in Ppt1-/- mice by NtBuHA: therapeutic implications for INCL. Nat. Neurosci. 2013; 16(11):1608-17. PMID: 24056696.
Saha A.*, Sarkar C.*, Singh S.P.*, Zhang Z., Munasinghe J., Peng S., Chandra G., Kong E., and Mukherejee A.B. The blood-brain barrier is disrupted in a mouse model of infantile neuronal ceroid lipofuscinosis: amelioration by resveratrol. Hum. Mol. Genet. 2012; 21(10):2233-44; PMID: 22331300. (*Contributed equally to this study)
Kim S-J*, Zhang Z*, Sarkar C*, Tsai P-C, Lee Y-C, Dye Louis, Mukherjee A B. Palmitoyl protein thioesterase-1 deficiency impairs synaptic vesicle recycling at nerve terminals, contributing to neuropathology in humans and mice. J. Clin. Invest. 2008; 118(9): 3075-3086 (*Contributed equally to this study)
Complete List of Published Work:
https://www.ncbi.nlm.nih.gov/myncbi/1hGgjDi4z7L5I/bibliography/public/
Research Interests
Traumatic brain injury (TBI) is one of the major causes of death and disability in young and aged populations. To date no effective therapy is available, mainly because of incomplete understanding of the molecular mechanisms of injury associated biochemical changes in the injured brain. Its pathophysiology is highly complex and is associated with severe oxidative stress and perturbation of lipid homeostasis. Peroxisome a cellular organelle plays an important role in regulating cellular lipid homeostasis and redox balance which are extremely important for cells like neurons. Peroxisomal dysfunction in peroxisomal biogenesis disorder has been shown to cause neurological impairment. Dysregulation in peroxisomal function has also been implicated in several neurodegenerative diseases. However, how peroxisomal function is regulated after TBI is not clearly know. Our preliminary data show that dysregulation in lipid metabolism in the mouse brain after controlled cortical impact (CCI) induced TBI. We detected reduced level of etherphospholipids and elevated level of very long chain fatty acids in the injured cortices of mouse following CCI-induced TBI using tandem liquid chromatography mass spectrometry (LC-MS/MS). These suggest that peroxisomal function is impaired in the injured brain. However, the exact mechanism of TBI induced peroxisomal dysregulation is not known. Currently, the focus of my study is to understand the mechanism of peroxisomal dysregulation following TBI both at the early acute phase and during aging. My research is also aimed to understand the role and functions of peroxisomal impairment in neurodegeneration and neuroinflammation in TBI and age associated neurodegenerative diseases.
Grants and Contracts
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2020-Present |
Role: Co-I “Dysregulation of autophagy-lysosomal function links TBI to late-onset neurodegeneration”. R01 (NS091218; PI: Lipinski) |
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2020-Present |
Role: PI “Role and Function of Ether Phospholipid and Peroxisome in TBI”. R21 (R21NS117867). |
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2019-Present |
Role: Co-PI Development of diagnostic biomarkers for determination of traumatic brain injury Grant Number: 3U01FD005946-03S3, FDA |
Professional Activity
- Member: Society for Neuroscience and National Neurotrauma Society
- Associate Editor: Neuroscience Letters
Lab Techniques and Equipment
- Controlled cortical impact (CCI) induced TBI model of mice
- Motor and cognitive assessment of mice using beam walk test and novel object recognition and Morris water maze tests
- Primary cortical neuron, astrocytes, microglia, bone marrow derived macrophage and neural stem cell culture
- Organelle (lysosome, peroxisome and mitochondria) isolation
- Immunoprecipitation, Western blot, Real-time qPCR, Immunostaining, FACS and enzyme assays
- Plasmid purification, cloning, transfection