Thomas Jefferson University - Jayasri Das Sarma
|
|
Jayasri Das Sarma
Neurology
Assistant Professor: 2004-2008
Adjunct Faculty: 2008-Till date
Department of Neurology
Thomas Jefferson University
Jefferson Medical College
Appointed: 2008
Present Affiliation:
Associate Professor (2008-till date)
Indian Institute of Science Education and Research-Kolkata( IISER-K)
India.
http://www.iiserkol.ac.in/faculty_homepages/JDS.html
Visiting Scientist
Neurology Department
Children Hospital of Philadelphia (CHOP)
Philadelphia, PA, USA
|
|
|
|
|
Mailing Address
|
302 JHN, 900 Walnut Street
Philadelphia, Pennsylvania 19107
United States
|
|
 |
|
|
Qualifications
|
B. Ed. Calcutta University, Kolkata, India; Teacher's Training, 1987
M. Phil. Calcutta University, Kolkata, India; Environmental Science, 1991
Ph.D., Javadpur University,Kolkata, India; Immunology/Chemistry, 1995
|
|
|
Expertise and Research Interests
|
A) Molecular and Cellular Virology: Neurological dysfunction is a manifestation of several neurodegenerative and autoimmune diseases of the nervous system, such as Alzheimer's disease, Parkinsons disease, HIV-1 associated encephalopathy and in Multiple Sclerosis (MS). Of these, MS is one of the most common demyelinating diseases of the human central nervous system (CNS) afflicting about 400,000 people in the United States, primarily in the age group of 20 to 45. The pathophysiological mechanisms underlying the changes in neurological function are as yet unresolved, but may include neuroinflammatory responses to infectious and/or environmental, as well as endogenous factors. My laboratory is interested in identifying and characterizing the molecular and cellular pathways involved in the neuroinflammatory mechanisms of MS, which can provide insights for therapeutic inventions.
Long standing hypotheses on the etiology of MS suggest that an infectious agent encountered during adolescence primes a disease process that later appears in the adult after a variable period of quiescence, when the viral particle may or may not be present. It is not known what can be the intervening stages between early age viral infection and later induction of demyelination. A better insight into the molecular and cellular mechanisms of these processes leading to MS lies in the systematic study of animal models. Towards this goal several experimental animal models have been developed to study the mechanisms of virus-induced demyelination, including the coronaviral mouse hepatitis virus (MHV) infection. Infection of mice with neurotropic strains of MHV induces a biphasic neurological disease with acute meningoencephalitis, followed by chronic inflammatory demyelination which mimics the pathology of MS. In MHV induced neuroinflammatory model, demyelination develops when virus is cleared and encephalitis is resolved. My research interest is focused on identifying the factors and the pathways used by the MHV to establish the acute stage encephalitis and the later stage disease process on two levels. First, what are the genomic controls of the early stage disease process? Here, using targeted RNA recombination we are generating recombinant strains of MHV with different encephalitic and demyelinating properties to study mouse CNS pathophysiology. Second, for mechanistic studies we use different phenotypic strains to understand how the variation in the genomic control (viral factors) can influence the later events of CNS cellular destruction processes. Understanding the correlation between the early stage of encephalitis and chronic stage demyelinating disease and the viral factors which may contribute to the disease progression is helping us to define pathway(s) underlying the pathological mechanism of MHV induced neuroinflammation.
The studies are being extended to human viruses that show high seropositivity during MS infection. Specific viral genes that interact with human locus are being targeted for virology and cell biology studies based on leads from bioinformatic analysis. By building parallels between mechanism of infection in human and mouse our goal is to build testable hypothesis that can help us gain better insight into MS and possibilities of better therapeutic intervention.
B)Cell biology of Gap junction protein (Connexin):
i)Intracellular trafficking and assembly of gap junction protein (Connexin) in the intracellular compartments.
ii)Looking for molecular chaperones for the quality control pathway of connexin 43 assembly in the intracellular compartments.
|
|
|
Keywords
|
|
Corona Viruses; Gap Junction; Multiple Sclerosis
|
|
|
Publications
|
- Marek, R, Caruso M, Rostami AM, Grinspan JB, Das Sarma J*. Magnetic cell sorting: a fast and effective method of concurrent isolation of high purity viable astrocytes and microglia from neonatal mouse brain tissue. Journal of Neuroscience Methods 175 (1) 108-118, October , 2008.
- Shindler KS, Kenyon LC, Dutt M, Hingley ST, Das Sarma J*. Experimental optic neuritis induced by a demyelinating strain of mouse hepatitis virus. J Virology, 82(17):8882-6, September, 2008.
- Das Sarma J*, Iacono K, Gard L, Marek R, Kenyon LC, Koval M, Weiss SR. Demyelinating and nondemyelinating strains of mouse hepatitis virus differ in their neural cell tropism. J Virology. 82(11):5519-26, June 2008.
- Das Sarma J, Kaplan BE, Willemsen D, Koval M. Identification of rab20 as a potential regulator of connexin 43 trafficking. Cell Commun Adhes, 15(1):65-74, May 2008.
- Fitzgerald D C., Ciric B, Touil T , Harle Hr , Grammatikopolou J, Das Sarma J, Gran B , Zhang G-X, Rostami A.M. Suppressive effect of IL-27 on encephalitogenic Th17 cells and the effector phase of experimental autoimmune encephalomyelitis (EAE). J. Immunol. 179 (5) 3268-75.2007.
- Qiu Z, Hingley ST, Simmons G, Yu C, Das Sarma J, Bates P, Weiss SR. Endosomal proteolysis by cathepsins is necessary for murine coronavirus mouse hepatitis virus type 2 spike-mediated entry. J. Virology 80(12):5768-76.2006.
- Das Sarma J, Das S and Koval M. Regulation of connexin 43 oligomerization is saturable. Cell Commun Adhes. 12 (5-6) 237-47. 2005
- Maza J, Das Sarma J and Koval M. Defining a minimal motif required to prevent connexin oligomerization in the endoplasmic reticulum. J. Biol.Chem. 280(22):21115-21.2005.
- Ransohoff, Maria Wysocka, Brendan Hilliard, Toshiki Fujioka, Sean Murphy, Patrick J Tighe, Jayasri Das Sarma, Giorgio Trinchieri, and Abdolmohamad Rostami. Astrocytes as antigen presenting cells: expression of IL-12/IL-23. J. Neurocytochemistry. 95:331-340.2005
- Fu L, Gonzales DM, Li Y, Das Sarma J and Lavi E. A combination of mutations in the S1 part of the spike glycoprotein gene in coronavirus MHV-A59 abolishes demyelination. J. Neurovirology 10: 41-51, 2004.
- Gonzales DM, Fu L, Li Y, Das Sarma J and Lavi E. Coronavirus induced demyelination occurs in the absence CD28 co-stimulatory signals. J. Neuro. Immunol. 146:140-143,2004.
- Maza J, Mateescu M, Das Sarma J and Koval M. Differential oligomerization of endoplasmic reticulum retained connexin 43/connexin 32 chimeras. Cell Commun. Adhesion. 10:319-322, 2003.
- Das Sarma J, Scheen E, Seo Su Hun, Koval M and Weiss SR. Enhanced green fluorescence protein expression may be used to monitor murine coronavirus spread in vitro and in the central nervous system. J. Neurovirology 8: 381-391, 2002.
- Das Sarma J, Wang F and Koval M. Targeted gap junction protein constructs reveal connexin specific differences in oligomerization. J. Biol. Chem. 277: 20911-20918, 2002.
- Das Sarma J, Meyer R, Wang F, Abraham V, Lo CW and Koval M. Multimeric connexin interactions prior to the trans golgi network. J. Cell Science 114: 4013-4024, 2001.
- Das Sarma J, Lo CW and Koval M. Cx43/b-gal inhibits Cx43 transport in the golgi apparatus. Cell Commun. Adhesion. 8: 249-252, 2001.
- Das Sarma J, Fu Li, Hingley ST, Lai MC and Lavi E. Sequence analysis of the S gene of recombinant MHV-2/A59 coronaviruses reveals three candidate mutations associated with demyelination and hepatitis. J. Neurovirology 7: 432-436, 2001.
- Das Sarma J, Fu Li, Hingley ST and Lavi E. Mouse hepatitis virus type-2 infection in mice: an experimental model system of acute meningitis and hepatitis. Exp. Mol. Pathology 71: 1-12, 2001.
- Navas S, Seo Su-hun, Chua MM, Das Sarma J, Lavi E, Hingley, ST, Weiss SR. The spike protein of murine coronavirus determines the ability of the virus to replicate in the liver and cause hepatitis. J. Virology 75: 2452-2457, 2001.
- Das Sarma J, Fu Li, Weiss SR and Lavi E. Demyelination determinants in the S gene of MHV. Adv. Exp. Med. Biol. 494: 133-135, 2001.
- Fu Li, Das Sarma J and Lavi E. Differential expression of tumor necrosis factor in primary glial cell cultures infected with demyelinating and non-demyelinating MHVs. Adv. Exp. Med. Biol. 494: 663-668, 2001.
- Das Sarma J, Fu Li, Tsai JC, Weiss SR and Lavi E. Demyelination determinants map to the spike glycoprotein gene of coronavirus mouse hepatitis virus. J. Virology 74: 9206-9213, 2000.
- Sengupta D, Duttagupta C, Bandyopadhyay S, Jana R, Das Sarma J, Sengupta S and Ray M. An exploratory statistical analysis of the effect of demographic risk factors on uterine cervical squamous interepithelial lesion. Calcutta Statistical Association Bulletin (Golden Jubilee Issue) 50: 307-324, 2000.
- Lavi E, Das Sarma J and Weiss SR. Cellular reservoirs for coronavirus infection of the brain in b2 microglobulin knock out mice. Pathobiology 67: 75-83, 1999.
- Das Sarma J, Duttagupta C, Ali E and Dhar TK. Improved microtiter plate based microbiological assay of folic acid with Streptococcus faecalis. J. AOAC International 78: 1173-1177, 1995.
- Das Sarma J, Duttagupta C, Ali E and Dhar TK. Direct microtiter plate enzyme immunoassay of folic acid without heat denaturation of serum. J. Immunological Methods 184: 1-6, 1995.
- Das Sarma J, Duttagupta C, Ali E and Dhar TK. Antibody to folic acid: increased specificity and sensitivity in ELISA by using e-amino caproic acid modified BSA as a carrier protein. J. Immunological Methods 184: 7-14, 1995.
|
|
Individual Expertise profile of
Jayasri Das Sarma, Copyright © Jayasri Das Sarma.
Last Updated
by Jayasri Das Sarma : Sunday, June 14, 2009 10:59:48 PM
|
|
|---|
|
|
|
|
