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Dr. Arup Banerjee

Associate Professor
E-mail: arup at rcb dot res dot in

  • M.Sc. (Biochemistry), University of Calcutta, Kolkata
  • Ph.D. (Life Sciences) 2007, Jadavpur University, Kolkata
  • Postdoc (2008-2010) at Saint Louis University, MO, USA
  • Research Scientist D (2011-Aug. 2018) at VIDRC, THSTI, Faridabad

Currently, our Laboratory is interested in deciphering the molecular events that trigger the pathways involved in the development of severe dengue. We will be exploring the following areas 1) Neutrophil Platelet interaction in context to endothelial barrier dysfunction and platelet apoptosis; (2) role of long non-coding RNAs in antiviral response; and (3) characterization of circulating exosomes and their role in the impairment of immune cell function

  • Neutrophil Platelet interaction in the context of endothelial barrier dysfunction
  • During severe condition, many of the critical dengue patients exhibit low virus titer suggesting that viral load is not an only determinant factor for disease severity. Instead, an imbalance in immune response may involve in the development of severity. Our recent transcriptomic analysis study on dengue patients further suggested that enhanced leukocyte migration and activation of neutrophil may associate with severe dengue. Involvement of neutrophils in dengue infection and disease progression not yet studied. Therefore, based on our previous study, we propose to explore the role of neutrophil activation pathway in dengue disease progression and will identify the critical molecules that trigger neutrophil activation process during severe condition.

  • Role of long non-coding RNAs in antiviral response
  • The noncoding RNAs (ncRNAs) can play a vital role in regulating gene expression in the infected immune cells and may help to develop pathogenesis. In our previous study, we have identified novel and annotated long noncoding RNAs (lncRNAs) associated with dengue disease progression. However, the mechanisms of action of the lncRNAs are unknown. A deeper understanding of functions and regulations of lncRNAs will further enhance our knowledge which will serve as a foundation for future translational research efforts.

  • Characterization of circulating exosomes and their role in the impairment of immune cell function
  • Severe dengue manifestation may be an outcome of impaired or altered function of immune cells. There is a growing body of evidence that exosomes, (small membrane vesicle) release from infected cells, may dampen the function of the immune cells. However, detail study is needed to comprehend the effect of circulating exosomes on immune modulation in the context of dengue infection and disease manifestation.


    Other projects are currently pursuing

    • Understanding the therapeutic role of adult stem cell-derived exosome in combating virus-induced neurodegenerative disease
    • Funded by: DBT, India, (BT/PR15984/MED/31/325/2015), Duration: 2018-2021
    • Principal investigators & collaborators: Dr. Anirban Basu, NBRC, Manesar; Dr. Sujata Mohanty, AIIMS, New Delhi; Dr. Arup Banerjee, RCB, Faridabad
  • Neurodegenerative diseases (NDs) are chronic degenerative diseases of the central nervous system (CNS) and affect 37 million people worldwide. NDs are the fourth leading cause of death in the developed countries and becoming increasingly prevalent in developing countries. The WHO predicts that by the year 2040, NDs will exceed cancer as the second leading cause of death following cardiovascular disease. However, despite of the advancement in the biological research, the development of therapeutics that target CNS has been hindered due to the poor efficacy to cross Blood Brain Barrier (BBB). To date, a number of techniques have been employed for drug delivery to the brain, but these are associated with poor efficacy and safety issues. The increasing evidences suggest that the mesenchymal stem cells (MSCs) mediated therapeutic effect can be achieved using exosome which can induce healing mechanism in a paracrine manner. Moreover, compared with cells, exosomes are more stable and have a lower possibility of immune rejection following in vivo allogeneic administration, and may provide an alternative therapy for various diseases. However, in order to use MSC-Exosome (MSC-EX) in translational research in human neurodegenerative patients, it is additionally required to clarify whether MSC Exosome and Extracellular Vesicle (EV) in general can able to enter the brain through crossing BBB. Therefore, the focus of this proposal is to examine biologically active exosomes from MSC (isolated from young apparently healthy donor) and establish a general strategy for the rational use of stem cell derived exosome as cell free therapy for neurodegenerative diseases.
    • Investigating the molecular modulators of microglial activation and their effect on JEV pathogenesis
    • Funded by: DST, SERB, India, (EMR/2017/001490) Duration: 2018-2021
  • Microglia, brain-resident macrophages, acts as the first line of defense and play key roles in mounting the proper innate and adaptive immune responses in the CNS. Microglia locates within the neurogenic niches; thus becoming attractive candidates for modulating neurogenesis in both the healthy and injured brain. The evidence suggests that microglia become activated both indirectly as a consequence of neuronal damage and directly as a result of infection of the microglia themselves. In the context of brain pathology, the microglial activation may lead to two phenotypic profiles: the classical M1 and the alternative M2 activation/deactivation state. The classical M1 activation occurs as microglia encounters a foreign antigen. The M2 phenotype is neuroprotective as it releases anti-inflammatory cytokines, neurotrophic factors, and helps to repair and to restructure of the damaged ECM in the brain. Few studies suggested that the nonspecific inflammatory blockade is unlikely to be beneficial for the disease treatment; rather, switching microglial activation towards neuroprotective phase may be advantageous to resolve inflammation. During acute brain inflammation, microglial activation is more dynamic; the transformation from M1 to M2 phase and the deactivation of microglia is delicately balanced to maintain the homeostasis. However, key molecules that control the switch is not defined. Therefore, Knowledge of the key molecules that regulate microglial activation in disease condition will open new avenues for a better therapeutic option for controlling virus-induced neuroinflammation.
    • Ms. Aarti Tripathi
      Ph.D. student
    • Ms. Naina Soni
      Junior Research Fellow
    • Received fellowship from ‘Viral Hepatitis Research Foundation of Japan’ in 2005 & 2011
    1. Pandey AD, Goswami S, Shukla S, Das S, Ghosal S, Pal M, Bandyopadhyay B, Ramachandran V, Basu N, Sood V, Pandey P, Chakrabarti J, Vrati S, Banerjee A. Correlation of altered expression of a long non-coding RNA, NEAT1, in peripheral blood mononuclear cells with dengue disease progression. J Infect. 2017 Oct 12. pii: S0163-4453(17)30308-0. doi: 10.1016/j.jinf.2017.09.016. PMID:29031635
    2. Banerjee A, Shukla S, Pandey AD, Goswami S, Bandyopadhyay B, Ramachandran V, Das S, Malhotra A, Agarwal A, Adhikari S, Rahman M, Chatterjee S, Bhattacharya N, Basu N, Pandey P, Sood V, Vrati S, RNA-Seq analysis of peripheral blood mononuclear cells reveals unique transcriptional signatures associated with disease progression in dengue patients, Transl Res. 2017 Aug;186:62-78.e9. doi: 10.1016/j.trsl.2017.06.007. Epub 2017 Jun 17. PMID:28683259.
    3. Kumari B, Jain P, Das S, Ghosal S, Hazra B, Trivedi AC, Basu A, Chakrabarti J, Vrati S, Banerjee A. Dynamic changes in global microRNAome and transcriptome reveal complex miRNA-mRNA regulated host response to Japanese Encephalitis Virus in microglial cells. Scientific Reports 2016 Feb 3;6:20263. doi: 10.1038/srep20263. PMID:26838068 Cited by 2
    4. Goswami S, Banerjee A, Kumari B, Bandyopadhyay B, Bhattacharya N, Basu N, Vrati S, Arup Banerjee. Differential expression and significance of circulating microRNAs in cerebrospinal fluid of acute encephalitis patients infected with Japanese Encephalitis Virus. Molecular Neurobiology 2016. PMID: 26860411 PMID: 26860411, DOI: 10.1007/s12035-016-9764-y
    5. Sarkar N, Panigrahi R, Pal A, Biswas A, Singh SP, Kar S, Bandyopadhyay M, Das D, Saha D, Kanda T, Sugiyama M, Chakrabarti S, Banerjee A , Chakravarty R. Expression of microRNA-155 correlates positively with the expression of Toll-Like Receptor 7 and modulates Hepatitis B Virus via C/EBP-β in Hepatocytes. J Viral Hepatitis 2015 Oct;22(10):817-27. Cited by: 7
    6. Pareek S, Roy S, Kumari B, Jain P, Banerjee A, Vrati S. miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses. J Neuroinflammation. 2014 May 29;11(1):97. PMID: 24885259, DOI 10.1186/1742-2094-11-97 Cited by: 19
    7. Bandyopadhyay M, Banerjee A, Sarkar N, Panigrahi R, Datta S, Pal A, Singh SP, Biswas A, Chakrabarti S, Chakravarty R. Tumor suppressor micro RNA miR-145 and on micro RNAs miR-21 and miR-222 expressions are differentially modulated by hepatitis B virus X protein in malignant hepatocytes. BMC Cancer. 2014 Sep 26;14:721. Cited by: 13
    8. Banerjee A, Mazumdar B, Meyer K, Di Bisceglie AM, Ray RB, Ray R. Transcriptional repression of C4 complement by hepatitis C virus proteins. J Virol. 2011; 85:4157-66. Cited by: 25 doi: 10.1128/JVI.02449-10.
    9. Banerjee A, Meyer K, Mazumdar B, Ray RB, Ray R. Hepatitis C virus differentially modulates activation of forkhead transcription factors and insulin-induced metabolic gene expression. J Virol. 2010,84:5936-46. Cited by: 32. doi: 10.1128/JVI.02344-09
    10. Ait-Goughoulte M, Banerjee A, Meyer K, Mazumdar B, Ray RB, Ray R. Hepatitis C virus core protein interacts with fibrinogen-β and attenuates cytokine stimulated acute phase response. Hepatology 2010,51:1505-13. Cited by: 25
    11. Ray R, Meyer k, Banerjee A, Basu A, Houghton M, Frey S, and Belshe RB. Characterization of antibodies induced by vaccination with hepatitis C virus envelope glycoproteins. J Infect Dis. 2010,202:862-6. Cited by: 47
    12. Banerjee A, Saito K, Meyer K, Banerjee S, Ait-Goughoulte M, Ray RB, Ray R. Hepatitis C Virus Core Protein and Cellular Protein HAX-1 Promotes 5-Fluorouracil Mediated Hepatocyte Growth Inhibition. J Virol. 2009;83:9663-71. Cited by: 21
    13. Banerjee A, Kurvanob F, Datta S, Chandra PK, Tanaka Y, Mizokami M, Bhattacharya SK, Chakravarty R. Phylogenetic relatedness and genetic diversity of HBV genotype strain isolated from Eastern India. J Med Virol. 2006;78:1164-74. Cited by: 108. 10.1002/jmv.20677
    14. Datta S, Banerjee A, Chandra PK, Mahapatra PK, Chakrabarti S, Chakravarty R. Drug trafficking routes and hepatitis B in injection drug users, Manipur, India. Emerg Infect Dis. 2006;12: 1954-7.Cited by: 19

     

    Dr. Arup Banerjee
    Associate Professor
    Regional Centre for Biotechnology
    NCR Biotech Science Cluster
    3rd Milestone, Faridabad-Gurgaon Expressway
    P.O. Box No. 3, Faridabad - 121 001
    Haryana (NCR Delhi), India
    E-mail: arup at rcb dot res dot in
    Phone: 91 129-2848852

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