Update Your ProfileAcademic Title:
Assistant Professor
Primary Appointment:
Anesthesiology
Additional Title:
Assistant Profesor
Location:
MSTF # 6-00
Phone (Primary):
(410) 706-5920
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 Shock Trauma and Anesthesiology Research center, 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
My research is focused on understanding the role and function of lipids and cellular organelles in neurodegeneration and neuroinflammation in traumatic brain injury (TBI) and age-associated neurodegenerative diseases. Our recent study demonstrated that the abundance of ether-phospholipids, an ether bond containing glycerophospholipids, is dysregulated in the mouse cortices after TBI. Ether-phospholipids are major components of the cellular membrane and play an important role in cellular signaling via their structural impact on the formation and function of lipid rafts. Their synthesis is regulated by the concerted functions of peroxisomes and endoplasmic reticulum. Our study demonstrates that ether-phospholipids dysregulation after TBI is at least in part caused by peroxisomal impairment.
Currently, we are exploring the role and function of peroxisomes in the pathophysiology of TBI and ways to develop novel treatment strategies to minimize neurodegeneration and neuroinflammation after TBI by restoring its function in the injured brain.
Grants and Contracts
|
2020-Present |
Role: Co-I “Dysregulation of autophagy-lysosomal function links TBI to late-onset neurodegeneration”. R01 (NS091218; PI: Lipinski) |
|
2020-Present |
Role: PI “Role and Function of Ether Phospholipid and Peroxisome in TBI”. R21 (R21NS117867). |
|
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