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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

Our Disease Biology 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, 3) diabetes and 4) hypobaric hypoxia-induced edema at high-altitude.

1) Hemolytic disorders: In hemolytic disorders 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 hyper-coagulative complications. The activated platelets and their cytokines further activate the leukocytes including monocytes, macrophages and neutrophils, and mediate the inflammatory complications. Further, we are investigating the molecular pathogenesis of the above clinical events using hemolytic mice models 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. Also, we have investigated that the platelet cytokine PF4 – mediated enhancement of replication as well as propagation of DV and also Japanese encephalitis virus (JEV) in host. Further, the inhibition of PF4 axis abrogated JEV infection in mice. Further, we are investigating the above mechanism in detail using transgenic mice models and also developing targeted therapeutics against PF4 for the treatment of these viruses in host.

3) Diabetes: We are studying the mechanism of platelet activation in type-2 diabetes (T2D) and also mechanisms of systemic as well as lung inflammations and lung fibrosis in patients as well as in transgenic mice model of the disease. Also, we are studying the mechanism, when the native highlanders migrate to lower altitudes, how they develop this metabolic disorder, T2D more often. Preliminary studies suggest that highlanders living in plan land develop more severe form of the disease. We are investigating the correlation between hypoxia-responsive factors and metabolites of glucose/fat oxidation pathways in the native and migrants (migrated from high to low altitudes) individuals.

4) Hypobaric hypoxia-induced edema: The high-altitude hypoxia increases the risk of edema (inflammation) and intravascular clot formation among the sojourners (travelers). However, the native highlanders including Tibetans are living normally at higher altitudes under extreme condition (where partial pO2 pressure less than 40% 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 mechanisms, how extreme hypoxic conditions trigger complications such as edema and blood clot formation in sojourners but not in native highlanders at high-altitudes.

  • Amrita Ojha
    Senior Research Fellow
    amrita.ojha@rcb.res.in
  • Angika Bhasym
    Senior Research Fellow
    angika.bhasym@rcb.res.in
  • Sulagna Bhattacharya
    Senior Research Fellow
    sulagna.sb@rcb.res.in
  • Srimali Nishith Maheshbhai
    Senior Research Fellow
    nishith@rcb.res.in
  • Saibal Saha
    Junior Research Fellow
    saibal@rcb.res.in
  • Sakshi Agarwal
    Junior Research Fellow
    sakshi.agarwal@rcb.res.in
  • Anamika Singh
    Junior Research Fellow
    sakshi.agarwal@rcb.res.in
  1. Bhasym A, Annarapu GK, Saha S, Shrimali N, Gupta S, Seth T, Guchhait P. (2019) Neutrophils develop rapid proinflammatory response after engulfing Hb-activated platelets under intravascular hemolysis. Clin Exp Immunol | Doi: 10.1111/cei.13310
  2. Bhakuni T, Singhal R, Aannarapu GK, Sharma A, Mahapatra M, Saxena R, Guchhait P (2019) Unique case of autoantibody mediated inactivation of ADAMTS13 in an Indian TTP patient. Blood Cells Molecules Diseases | 77:29-33
  3. Bhasym A, Gurjar BS, Sriharsha TM, Bhasym A, Prabhu S, Puraswani M, Khandelwal P, Saini H, Saini S, Verma AK, Chatterjee P, Bal V, George A, Sharma A, Hari P, Sinha A, Bagga A, Rath S, Guchhait P (2019) Altered Peripheral Blood Leucocyte Phenotype and Responses in Healthy Individuals with Homozygous Deletion of FHR1 and FHR3 Gene. J Clinical Immunology | Doi.org/10.1007/s10875-019-00619-2
  4. R Singhal, DK Rathore, T Bhakuni, T Seth, P Guchhait (2019) Absence of Nonclassical Monocytes in Hemolytic Patients : Free Hb and NO-Mediated Mechanism Journal of Immunology Research | doi.org/10.1155/2019/1409383
  5. Ojha A, Bhasym A, Mukherjee S, Annarapu GK, Bhakuni T, Akbar I, Seth T, Vikram NK, Vrati S, Basu A, Bhattacharyya S, Guchhait P. Platelet factor 4 promotes rapid replication and propagation of Dengue and Japanese encephalitis viruses. EBioMedicine 2018 | 39:332-347
  6. 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]
  7. 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
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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
  13. 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]
  14. 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]
  15. Pandey A, Chawla S, Guchhait P (2015)  Type-2 diabetes: Current understanding and future perspectives. IUBMB Life 67:506
  16. 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.
  17. 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.
  18. 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.
  19. 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
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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