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Peter H. Lapchak, Ph.D.

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Biography
1985 - 1986
Fonds pour la Formation de Chercheurs et l’Aide Recherche (FCAR)
1989 - 1992
Canadian Diabetes Association (Edmonton Branch), J. B. Collip Diabetes Studentship
1989 - 1989
Juvenile Diabetes Foundation (US) Summer Student Award
1993 - 1993
Mary Louise Imrie Student Travel Award, Faculty of Graduate Studies and Research, U. Alberta
1995 - 1995
Society for Leukocyte Biology Travel Award
1997 - 1998
Joseph E. Murrray Award, National Kidney Foundation Massachusetts and Rhode Island Affiliate
1998 - 2000
American Heart Association-Massachusetts Affiliate Fellowship
2002 - 2003
Pediatric Renal Research Award, National Kidney Foundation of Massachusetts, RI, NH, VT Affiliate
2005 - 2006
Surgical Infection Society (SIS) Junior Faculty Research Fellowship Award
2006 - 2007
Surgical Infection Society (SIS) Junior Faculty Research Fellowship Award Competitive Renewal
2009 - 2011
Department of Defense Research Grant
2009 - 2011
Department of Defense Research Grant

Overview
My research interests over the last 8 years has been to decipher the role of platelets in immune responses and inflammation using animal models of local and systemic trauma, namely ischemia-reperfusion and thermal injury. Platelets have many features in common with classical immune cells such as monocytes and lymphocytes although they are devoid of a nucleus. They are capable of secreting cytokines and express cell surface molecules that are common on immune cells. Although platelets are typically pro-inflammatory in nature, they may also be protective to the host after severe trauma by dampening the pro-inflammatory cascade. Thus, platelets may modulate the host response to systemic injury such as that observed in burn injury. In contrast, platelets may be detrimental to the host after severe local trauma such as that observed in ischemia-reperfusion injury. My overall goals are 1) to identify the differences in platelet responses and platelet-mediated immune responses after systemic or local trauma, 2) to determine the signaling pathways important in platelet activation in response to these different modes of injury, 3) identify differences in platelet subsets and their origins, and 4) understand the role of platelets in systemic and organ-specific autoimmune disease.

Platelets may associate with soluble factors such as those of the complement system and with immunoglobulins. Another aspect of my research involves identifying specific factors that associate with platelets and determine if, together they mediate tissue injury and organ damage. Ultimately, developing diagnostic tools to identify inappropriate platelet activation and pharmacotherapeutic and biotherapeutic agents to dampen or prevent tissue injury are realistic goals.

Bibliographic
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
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PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
  1. Satyam A, Andreo K, Lapchak PH, Dalle Lucca JJ, Davis RB, Tsokos MG, Shapiro NI, Tsokos GC. Complement Deposition on the Surface of RBC After Trauma Serves A Biomarker of Moderate Trauma Severity: A Prospective Study. Shock. 2019 Apr 12. PMID: 30998651.
    Citations:    
  2. Matsumoto N, Satyam A, Geha M, Lapchak PH, Dalle Lucca JJ, Tsokos MG, Tsokos GC. C3a Enhances the Formation of Intestinal Organoids through C3aR1. Front Immunol. 2017; 8:1046. PMID: 28928734.
    Citations:    
  3. Bialas AR, Presumey J, Das A, van der Poel CE, Lapchak PH, Mesin L, Victora G, Tsokos GC, Mawrin C, Herbst R, Carroll MC. Microglia-dependent synapse loss in type I interferon-mediated lupus. Nature. 2017 06 22; 546(7659):539-543. PMID: 28614301.
    Citations: 14     Fields:    Translation:HumansAnimalsCells
  4. Satyam A, Kannan L, Matsumoto N, Geha M, Lapchak PH, Bosse R, Shi GP, Dalle Lucca JJ, Tsokos MG, Tsokos GC. Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia. J Immunol. 2017 01 15; 198(2):788-797. PMID: 27913632.
    Citations: 7     Fields:    Translation:HumansAnimalsCells
  5. Lapchak PH, Ioannou A, Rani P, Lieberman LA, Yoshiya K, Kannan L, Dalle Lucca JJ, Kowalska MA, Tsokos GC. The role of platelet factor 4 in local and remote tissue damage in a mouse model of mesenteric ischemia/reperfusion injury. PLoS One. 2012; 7(7):e39934. PMID: 22792197.
    Citations: 10     Fields:    Translation:AnimalsCells
  6. Lapchak PH, Kannan L, Rani P, Pamuk ON, Ioannou A, Dalle Lucca JJ, Pine P, Tsokos GC. Inhibition of Syk activity by R788 in platelets prevents remote lung tissue damage after mesenteric ischemia-reperfusion injury. Am J Physiol Gastrointest Liver Physiol. 2012 Jun 15; 302(12):G1416-22. PMID: 22492694.
    Citations: 2     Fields:    Translation:AnimalsCells
  7. Lapchak PH, Ioannou A, Kannan L, Rani P, Dalle Lucca JJ, Tsokos GC. Platelet-associated CD40/CD154 mediates remote tissue damage after mesenteric ischemia/reperfusion injury. PLoS One. 2012; 7(2):e32260. PMID: 22384195.
    Citations: 6     Fields:    Translation:AnimalsCells
  8. Lapchak PH, Kannan L, Ioannou A, Rani P, Karian P, Dalle Lucca JJ, Tsokos GC. Platelets orchestrate remote tissue damage after mesenteric ischemia-reperfusion. Am J Physiol Gastrointest Liver Physiol. 2012 Apr 15; 302(8):G888-97. PMID: 22301111.
    Citations: 8     Fields:    Translation:AnimalsCells
  9. Yoshiya K, Lapchak PH, Thai TH, Kannan L, Rani P, Dalle Lucca JJ, Tsokos GC. Depletion of gut commensal bacteria attenuates intestinal ischemia/reperfusion injury. Am J Physiol Gastrointest Liver Physiol. 2011 Dec; 301(6):G1020-30. PMID: 21903760.
    Citations: 27     Fields:    Translation:Animals
  10. Pamuk ON, Lapchak PH, Rani P, Pine P, Dalle Lucca JJ, Tsokos GC. Spleen tyrosine kinase inhibition prevents tissue damage after ischemia-reperfusion. Am J Physiol Gastrointest Liver Physiol. 2010 Aug; 299(2):G391-9. PMID: 20522642.
    Citations: 15     Fields:    Translation:AnimalsCells
  11. Fujimi S, Lapchak PH, Zang Y, MacConmara MP, Maung AA, Delisle AJ, Mannick JA, Lederer JA. Murine dendritic cell antigen-presenting cell function is not altered by burn injury. J Leukoc Biol. 2009 May; 85(5):862-70. PMID: 19228816.
    Citations: 7     Fields:    Translation:AnimalsCells
  12. Shi T, Moulton VR, Lapchak PH, Deng GM, Dalle Lucca JJ, Tsokos GC. Ischemia-mediated aggregation of the actin cytoskeleton is one of the major initial events resulting in ischemia-reperfusion injury. Am J Physiol Gastrointest Liver Physiol. 2009 Feb; 296(2):G339-47. PMID: 19095765.
    Citations: 8     Fields:    Translation:AnimalsCells
  13. MacConmara MP, Maung AA, Fujimi S, McKenna AM, Delisle A, Lapchak PH, Rogers S, Lederer JA, Mannick JA. Increased CD4+ CD25+ T regulatory cell activity in trauma patients depresses protective Th1 immunity. Ann Surg. 2006 Oct; 244(4):514-23. PMID: 16998360.
    Citations: 42     Fields:    Translation:HumansCells
  14. Fujimi S, MacConmara MP, Maung AA, Zang Y, Mannick JA, Lederer JA, Lapchak PH. Platelet depletion in mice increases mortality after thermal injury. Blood. 2006 Jun 01; 107(11):4399-406. PMID: 16467203.
    Citations: 16     Fields:    Translation:AnimalsCells
  15. Flaxenburg JA, Melter M, Lapchak PH, Briscoe DM, Pal S. The CD40-induced signaling pathway in endothelial cells resulting in the overexpression of vascular endothelial growth factor involves Ras and phosphatidylinositol 3-kinase. J Immunol. 2004 Jun 15; 172(12):7503-9. PMID: 15187129.
    Citations: 14     Fields:    Translation:HumansCells
  16. Lapchak PH, Melter M, Pal S, Flaxenburg JA, Geehan C, Frank MH, Mukhopadhyay D, Briscoe DM. CD40-induced transcriptional activation of vascular endothelial growth factor involves a 68-bp region of the promoter containing a CpG island. Am J Physiol Renal Physiol. 2004 Sep; 287(3):F512-20. PMID: 15140761.
    Citations: 6     Fields:    Translation:HumansCells
  17. Frank NY, Pendse SS, Lapchak PH, Margaryan A, Shlain D, Doeing C, Sayegh MH, Frank MH. Regulation of progenitor cell fusion by ABCB5 P-glycoprotein, a novel human ATP-binding cassette transporter. J Biol Chem. 2003 Nov 21; 278(47):47156-65. PMID: 12960149.
    Citations: 64     Fields:    Translation:HumansCells
  18. Lapchak PH, Briscoe DM. Hyporesponsiveness in pediatric recipients. Pediatr Transplant. 2002 Feb; 6(1):8-11. PMID: 11906635.
    Citations:    Fields:    Translation:Humans
  19. Pellegrini JD, Puyana JC, Lapchak PH, Kodys K, Miller-Graziano CL. A membrane TNF-alpha/TNFR ratio correlates to MODS score and mortality. Shock. 1996 Dec; 6(6):389-96. PMID: 8961387.
    Citations: 7     Fields:    Translation:HumansCellsCTClinical Trials
  20. Pelligrini M.D., J., J.C. Puyana M.D., A. De Ph.D., G. Fudem M.D., K. Kodys B.A., P. Lapchak Ph.D., and C. Miller Ph.D. A Trauma Induced T Cell Defect is Associated with Deregulated Monokine Production and Is Truly Predictive of Poor Clinical Outcome. Surgical Forum. 1996; XLVII:64-66.
  21. Rabinovitch A, Suarez-Pinzon WL, Lapchak PH, Meager A, Power RF. Tumor necrosis factor mediates the protective effect of Freund's adjuvant against autoimmune diabetes in BB rats. J Autoimmun. 1995 Jun; 8(3):357-66. PMID: 7575997.
    Citations: 2     Fields:    Translation:Animals
  22. Garner R, Helgason CD, Atkinson EA, Pinkoski MJ, Ostergaard HL, Sorensen O, Fu A, Lapchak PH, Rabinovitch A, McElhaney JE, et al. Characterization of a granule-independent lytic mechanism used by CTL hybridomas. J Immunol. 1994 Dec 15; 153(12):5413-21. PMID: 7527440.
    Citations: 7     Fields:    Translation:AnimalsCells
  23. Wride MA, Lapchak PH, Sanders EJ. Distribution of TNF alpha-like proteins correlates with some regions of programmed cell death in the chick embryo. Int J Dev Biol. 1994 Dec; 38(4):673-82. PMID: 7779688.
    Citations: 9     Fields:    Translation:Animals
  24. Lapchak PH, Guilbert LJ, Rabinovitch A. Tumor necrosis factor production is deficient in diabetes-prone BB rats and can be corrected by complete Freund's adjuvant: a possible immunoregulatory role of tumor necrosis factor in the prevention of diabetes. Clin Immunol Immunopathol. 1992 Nov; 65(2):129-34. PMID: 1395129.
    Citations: 7     Fields:    Translation:AnimalsCells
  25. Issa-Chergui B, Goldner-Sauvé A, Colle E, Prud'homme GJ, Lapchak PH, van der Meide PH, Seemayer TA. Class I and II major histocompatibility complex gene product expression by a rat insulinoma cell line in vitro following exposure to gamma interferon. Diabetologia. 1988 Sep; 31(9):675-80. PMID: 2853088.
    Citations: 1     Fields:    Translation:AnimalsCells
  26. Prud'homme GJ, Lapchak PH, Parfrey NA, Colle E, Guttmann RD. Autoimmunity-prone BB rats lack functional cytotoxic T cells. Cell Immunol. 1988 Jun; 114(1):198-208. PMID: 3131022.
    Citations: 1     Fields:    Translation:AnimalsCells
  27. Herrington MB, Kohli A, Lapchak PH. Suppression by thymidine-requiring mutants of Escherichia coli K-12. J Bacteriol. 1984 Jan; 157(1):126-9. PMID: 6360992.
    Citations: 3     Fields:    Translation:Cells
  28. Herrington MB, Lapchak PH, Kohli A. Suppression by an Escherichia coli mutant under thymine-limiting conditions. Mutat Res. 1983 Feb; 119(2):109-11. PMID: 6338364.
    Citations: 1     Fields:    Translation:Cells
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Funded by the NIH/NCATS Clinical and Translational Science Award (CTSA) program, grant number UL1TR001102, and through institutional support from Harvard University, Harvard Medical School, Harvard T.H. Chan School of Public Health, Beth Israel Deaconess Medical Center, Boston Children's Hospital, Brigham and Women's Hospital, Massachusetts General Hospital and the Dana Farber Cancer Institute.