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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 immunomodulatory role of platelets (thrombocytes), specifically how the platelet proteins and cytokines regulate the function of immune cells under various diseases and stress conditions.

Platelets play major role in maintaining hemostasis to stop bleeding from injured vessels, on the other hand, promote thrombosis or clot formation at intravascular space under various disease conditions. We are currently investigating the pathophysiology of hemolytic disorders including PNH, SCD, Thalassemia and HUS with a focus, how cell-free hemoglobin (Hb) activates platelets and promotes the pathogenesis of thrombosis, hypercoagulable states and inflammations. Besides, how the platelet proteins and cytokines are modulating the function of innate as well as adaptive immune cells in these patients. Also investigating the role of Hbplatelet-immune axis in the above clinical events using the mice models.

We are investigating the pathogenesis of thrombocytopenia in dengue infection with a focus, how the virus modulates platelet activation and how the platelet proteins regulate the viral propagation and modulate immune responses in patients and in mice.

We are investigating how the sojourners develop edema and intravascular clot formation when travel to high altitudes. To address the above, we are assessing the profiles of thrombocoaguation as well as inflammatory and immune parameters in native Tibetans from high altitudes, since majority of them carry the adaptive mutations that protects from extreme hypoxic environments. Recently we have described such novel mutations (C12G and G380C) in EGLN1 gene, which is the negative regulator of the master hypoxia sensor, hypoxia inducible factor (HIF)1α.

We are working on the mechanism, how the dynamic balance between complement factor H (CFH) and CFH-related protein (CFHR) maintains immune responses, since both are known to protect the host cells from complement activation as well as complement/immune attacks. Interestingly, a report describes that 80 percent of India pediatric patients with aHUS, a disease characterized by uncontrolled complement activation and autoimmune events have the CFHR1-3 deletion mutations. Besides, 10 percent of so-called healthy individuals also carry this mutation. We are investigating how both types of above individuals (CFHR1-3 null) are maintaining the immune tolerance.

  • 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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