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Dr. Prasenjit Guchhait

Professor
E-mail: prasenjit at rcb dot res dot in

  • PhD 1998, Banaras Hindu University
  • Postdoc at Baylor College of Medicine, USA
  • Instructor at Baylor College of Medicine, USA
  • Assistant Professor at Baylor College of Medicine, USA
  • Associate Professor at Regional Centre for Biotechnology, India

Currently our laboratory is focused on elucidating the role of platelets and leukocytes, and their molecules in the pathogenesis of events such as hyper-coagulation, thrombosis and inflammation, and immune responses under various conditions such as
1) hemolytic diseases, 2) viral infections and 3) high-altitude hypoxia.

1) Hemolytic disorders: In hemolytic disorders such as in including aplastic anemia, paroxysmal nocturnal hemoglobinuria (PNH), hemolytic uremic syndrome (HUS), thalassemia and sickle cell disease (SCD) the free-hemoglobin (Hb) in plasma triggers many cytotoxic effects. We have described that the free-Hb activates the circulating platelets potently and promotes pro-thrombotic as well as hypercoagulative complications. The activated platelets and their cytokines further activate the leukocytes including monocytes, macrophages and neutrophils, and mediate the inflammatory complications. Further, we are elucidating the detail mechanism of the above using hemolytic mice as well as patients samples.

2) Viral infections: In dengue virus (DV) infection, the platelets play significant role in thrombocytopenia as well as regulate immune responses in patients. We have shown that the platelet activation by DV is a crucial determinant of the thrombocytopenia in patients. The highly activated platelets showed higher chances of clearance from circulation. We also have investigated that the platelet cytokines triggers the rapid replication as well as propagation of DV in host cells. Further, we are investigating the role of various platelet proteins, detected from our proteome data, in the pathogenesis of viral infections in general.

3) High-altitude hypoxia: The high-altitude hypoxia increases the risk of edema and intravascular clot formation among the sojourners (travellers). However the native highlanders including Tibetans are living normally at higher altitudes under even less than 40% pO2 pressure (compared to sea-level). Recently we have described that the novel mutations (C12G and G380C) in EGLN1 gene (which encodes Prolyl Hydroxylase-2 (PHD2), the negative regulator of hypoxia inducible factor (HIF)1α (which is the master sensor of oxygen in our body), supports the adaptation of the native Tibetans at high altitudes. Basically the gain-in-function mutations help in maintenance of normal erythropoiesis (production of red blood cells) in these highlanders. Further, we are studying the mechanism of crosstalk between platelets and leukocytes in developing the symptoms such edema in the absence of these mutations. Also we are studying the mechanism, in the presence of these mutations how the Tibetans are protected from hyper-inflammatory as well as hyper-thrombotic responses under extreme hypoxic conditions.

  • Teena Bhakuni, PhD
    SERB NPDF
    teena@rcb.ac.in
  • Rashi Singhal
    Senior Research Fellow
    rashi@rcb.ac.in
  • Amrita Ojha
    Senior Research Fellow
    amrita.ojha@rcb.res.in
  • Angika Bhasym
    Senior Research Fellow
    angika.bhasym@rcb.res.in
  • Sulagna Bhattacharya
    Junior Research Fellow
    sulagna.sb@rcb.res.in
  • Srimali Nishith Maheshbhai
    Junior Research Fellow
    nishith@rcb.res.in
  • Saibal Saha
    Junior Research Fellow
    saibal@rcb.res.in
  • Jaya Saini
    Junior Research Fellow
    jaya@rcb.res.in
  1. Singhal R, Chawla S, Batra H, Gupta S, Ojha A, Rathore DK, Seth T, Guchhait P (2018) Engulfment of Hb-activated platelets differentiates monocytes into pro-inflammatory macrophages in PNH patients. Eur J Immunol. [Epub ahead of print]
  2. Gurjar BS, Sriharsha TM, Bhasym A, Prabhu S, Puraswani M, Khandelwal P, Saini H, Saini S, Verma AK, Chatterjee P, Gucchait P, Bal V, George A, Rath S, Sahu A, Sharma A, Hari P, Sinha A, Bagga A. (2018) Characterization of genetic predisposition and autoantibody profile in atypical hemolytic uremic syndrome. Immunology
  3. Tashi T, Reading N S, Wuren T, Zhang X, Moore L G, Hu H, Tang F, Shestakova A, Lorenzo F, Burjanivova T, Koul P, Guchhait P, Wittwer C T, Julian C G, Shah B, Huff C D, Gordeuk V R, Prchal J T, Ge R (2017) Gain-of-function EGLN1 prolyl hydroxylase (PHD2 D4E:C127S)in combination with EPAS1 (HIF-2α) polymorphism lowershemoglobin concentration in Tibetan highlanders J Mol Med 95-665
  4. Ojha A , Nandi D, Batra H, Singhal R, Annarapu G. K., Bhattacharyya. S, Seth T, Dar L, Medigeshi G. R., Vrati S, Vikram N. K & Guchhait P (2017) Platelet activation determines the severity of thrombocytopenia in dengue infection Sci Rep 7: 41697
  5. Singhal R, Chawla S, Rathore D K, Bhasym A, Annarapu G K, Sharma V, Seth T, Guchhait P (2016)Development of pro-inflammatory phenotype in monocytes after engulfing Hb-activated platelets in hemolytic disorders.. Clinical Immunology 12: 007
  6. Annarapu GK, Singhal R, Gupta A, Chawla S, Batra H, Seth T, Guchhait P (2016) HbS Binding to GP1ba Activates Platelets in Sickle Cell Disease.. PLoS One 11:e0167899
  7. Annarapu GK, Singhal R, Peng Y, Guchhait P. (2016) Inhibition of Hb binding to GP1bα abrogates Hb-mediated thrombus formation on immobilized VWF and collagen under physiological shear stress. PLoS One. 11:e0154276
  8. Singhal R, Annarapu GK, Pandey A, Chawla S, Ojha A, Gupta A, Cruz MA, Seth T, Guchhait P. (2015)  Hemoglobin interaction with GP1ba induces platelet activation and apoptosis: a novel mechanism associated with intravascular hemolysis. Haematologica. pii: haematol.132183. [Epub ahead of print]
  9. Da Q, Teruya M, Guchhait P, Teruya J, Olson JS, Cruz MA (2015)  Free hemoglobin increases von Willebrand factor-mediated platelet adhesion in vitro: implications on circulatory devices. Blood. pii: blood-2015-05-648030. [Epub ahead of print]
  10. Pandey A, Chawla S, Guchhait P (2015)  Type-2 diabetes: Current understanding and future perspectives. IUBMB Life 67:506
  11. Lorenzo FR, Huff C, Myllymäki M, Olenchock B, Swierczek S, Tashi T, Gordeuk V, Wuran T, Li GR, McClain DL, Khan TM, Koul PA, Guchhait P, Salama ME, Xing J, Semenz GL, Liberzon E, Wilson A, Simonson TS, Jorde LB, KaelinJr WG, Koivunen P, Prchal JT. (2014) A genetic mechanism for Tibetan high-altitude adaptation. Nature Genetics 46:951.
  12. Zhou Z, Thiagarajan P, Udden MA, Lopez JA, Guchhait P. (2011) Membrane sulfatide plays a crucial role in the sickle erythrocytes adhesion to matrix and endothelial ligands. Thrombosis Haemostasis105:1046.
  13. Zhou Z, Han H, Cruz MA, Jose JA, Dong JF, Guchhait P. (2009) Hemoglobin blocks von Willebrand factor proteolysis by ADAMTS-13: a mechanism associated with sickle cell disease. Thrombosis Haemostasis 101 (6):1070.
  14. Guchhait P, Shrimpton C, Honke K, Rumbaut R, Lopez JA, Thiagarajan P. (2008) Effects of an anti-sulfatide single-chain antibody probe on platelet function. Thrombosis Haemostasis 99(3):552.

Dr. Prasenjit Guchhait
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: prasenjit at rcb dot res dot in
Phone: 91 129-2848821

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