Craig N Morrell

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi In vivo platelet-endothelial cell interactions in response to major histocompatibility complex alloantibody
    Craig N Morrell
    Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 102:777-85. 2008
  2. ncbi Glutamate mediates platelet activation through the AMPA receptor
    Craig N Morrell
    Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Exp Med 205:575-84. 2008
  3. ncbi HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 96:1185-92. 2005
  4. ncbi Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factor
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Cell Biol 170:73-9. 2005
  5. ncbi Aldosterone activates endothelial exocytosis
    Youngtae Jeong
    Department of Medicine, Graduate Program in Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 106:3782-7. 2009
  6. ncbi Exocytosis of endothelial cells is regulated by N-ethylmaleimide-sensitive factor
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Methods Mol Biol 440:203-15. 2008
  7. ncbi Platelet kainate receptor signaling promotes thrombosis by stimulating cyclooxygenase activation
    Henry Sun
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Circ Res 105:595-603. 2009
  8. ncbi Regulation of Weibel-Palade body exocytosis
    Charles J Lowenstein
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Trends Cardiovasc Med 15:302-8. 2005
  9. ncbi Platelet factor 4 mediates inflammation in experimental cerebral malaria
    Kalyan Srivastava
    Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, 733 North Broadway, Baltimore, MD 21205, USA
    Cell Host Microbe 4:179-87. 2008
  10. ncbi Platelets contribute to allograft rejection through glutamate receptor signaling
    AnneMarie F Swaim
    Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Immunol 185:6999-7006. 2010

Research Grants

Collaborators

Detail Information

Publications22

  1. ncbi In vivo platelet-endothelial cell interactions in response to major histocompatibility complex alloantibody
    Craig N Morrell
    Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 102:777-85. 2008
    ..Taken together, our model demonstrates an important role for platelets in alloantibody induced transplant rejection...
  2. ncbi Glutamate mediates platelet activation through the AMPA receptor
    Craig N Morrell
    Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Exp Med 205:575-84. 2008
    ..Importantly, mice lacking GluR1 have a prolonged time to thrombosis in vivo. Our data identify glutamate as a regulator of platelet activation, and suggest that the AMPA receptor is a novel antithrombotic target...
  3. ncbi HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 96:1185-92. 2005
    ..These findings may explain part of the pleiotropic effects of statin therapy for patients with cardiovascular disease...
  4. ncbi Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factor
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Cell Biol 170:73-9. 2005
    ..Increasing endogenous H(2)O(2) levels in mice decreases exocytosis and platelet rolling on venules in vivo. By inhibiting endothelial cell exocytosis, endogenous H(2)O(2) may protect the vasculature from inflammation and thrombosis...
  5. ncbi Aldosterone activates endothelial exocytosis
    Youngtae Jeong
    Department of Medicine, Graduate Program in Pathobiology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 106:3782-7. 2009
    ..Aldosterone antagonism may decrease vascular inflammation and cardiac fibrosis in part by blocking endothelial exocytosis...
  6. ncbi Exocytosis of endothelial cells is regulated by N-ethylmaleimide-sensitive factor
    Munekazu Yamakuchi
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Methods Mol Biol 440:203-15. 2008
    ..Further characterization of the factors that regulate exocytosis will lead to novel treatments for vascular diseases such as myocardial infarction and stroke...
  7. ncbi Platelet kainate receptor signaling promotes thrombosis by stimulating cyclooxygenase activation
    Henry Sun
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Circ Res 105:595-603. 2009
    ..Each is well characterized in the central nervous system, but glutamate has important signaling roles in peripheral tissues as well, including a role in regulating platelet function...
  8. ncbi Regulation of Weibel-Palade body exocytosis
    Charles J Lowenstein
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Trends Cardiovasc Med 15:302-8. 2005
    ..This review examines the regulation of WPB exocytosis-the exocytic machinery, activators, and inhibitors of exocytosis-and speculates about the development of novel anti-exocytic drugs...
  9. ncbi Platelet factor 4 mediates inflammation in experimental cerebral malaria
    Kalyan Srivastava
    Department of Molecular and Comparative Pathobiology, The Johns Hopkins University School of Medicine, 733 North Broadway, Baltimore, MD 21205, USA
    Cell Host Microbe 4:179-87. 2008
    ..We conclude that Plasmodium-infected RBCs can directly activate platelets, and platelet-derived PF4 then contributes to immune activation and T cell trafficking as part of the pathogenesis of ECM...
  10. ncbi Platelets contribute to allograft rejection through glutamate receptor signaling
    AnneMarie F Swaim
    Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    J Immunol 185:6999-7006. 2010
    ....
  11. ncbi A novel inhibitor of N-ethylmaleimide-sensitive factor decreases leukocyte trafficking and peritonitis
    Craig N Morrell
    Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Pharmacol Exp Ther 314:155-61. 2005
    ..These data suggest that NSF is a critical regulator of leukocyte trafficking in vivo. Novel compounds that inhibit the exocytic machinery in endothelial cells may be useful anti-inflammatory drugs...
  12. ncbi Immunological challenges of cardiac transplantation: the need for better animal models to answer current clinical questions
    Jennifer R Wehner
    Department of Pathology, Johns Hopkins Medical Institutes, Baltimore, MD, USA
    J Clin Immunol 29:722-9. 2009
    ..First, more sensitive diagnostic tests for detection of AMR have been developed. Second, improvements in immunosuppression have made severe acute cellular rejection uncommon, but have had less effect on AMR...
  13. ncbi Beta interferon suppresses the development of experimental cerebral malaria
    Craig N Morrell
    Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
    Infect Immun 79:1750-8. 2011
    ..berghei-infected mice also had fewer brain T-cell infiltrates, further demonstrating its protective effects. Hence, IFN-? has important anti-inflammatory properties that ameliorate the severity of ECM and prolong mouse survival...
  14. ncbi Sphingosine 1-phosphate activates Weibel-Palade body exocytosis
    Kenji Matsushita
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 101:11483-7. 2004
    ..Thus S1P plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of S1P...
  15. ncbi Ceramide triggers Weibel-Palade body exocytosis
    Rinky Bhatia
    Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Circ Res 95:319-24. 2004
    ..These data suggest a novel mechanism by which ceramide induces vascular inflammation and thrombosis...
  16. ncbi Nitric oxide regulates exocytosis by S-nitrosylation of N-ethylmaleimide-sensitive factor
    Kenji Matsushita
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Cell 115:139-50. 2003
    ..NO may regulate exocytosis in a variety of physiological processes, including vascular inflammation, neurotransmission, thrombosis, and cytotoxic T lymphocyte cell killing...
  17. ncbi Antibody and complement in transplant vasculopathy
    Jennifer Wehner
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
    Circ Res 100:191-203. 2007
    ..The effect of these treatment modalities on the development of coronary vasculopathy is unknown...
  18. ncbi Vascular endothelial growth factor regulation of Weibel-Palade-body exocytosis
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Blood 105:207-14. 2005
    ..Thus, VEGF plays a dual role in regulating endothelial exocytosis, triggering pathways that both promote and inhibit endothelial exocytosis. Regulation of endothelial exocytosis may explain part of the proinflammatory effects of VEGF...
  19. ncbi Regulation of platelet granule exocytosis by S-nitrosylation
    Craig N Morrell
    Department of Comparative Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 102:3782-7. 2005
    ..Platelets lacking endothelial NO synthase show increased rolling on venules, increased thrombosis in arterioles, and increased exocytosis in vivo. Regulation of exocytosis is thus a mechanism by which NO regulates thrombosis...
  20. ncbi A novel class of fusion polypeptides inhibits exocytosis
    Kenji Matsushita
    Department of Medicine, The Johns Hopkins University School of Medicine, 950 Ross Building, 720 Rutland Avenue, Baltimore, MD 21205, USA
    Mol Pharmacol 67:1137-44. 2005
    ..These TAT-NSF compounds may be useful in the treatment of a variety of diseases in which exocytosis plays a prominent role, including myocardial infarction, stroke, thrombosis, and autoimmune disorders...
  21. ncbi Heterozygous disruption of Hic1 predisposes mice to a gender-dependent spectrum of malignant tumors
    Wen Yong Chen
    Division of Tumor Biology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins Medical Institutions, 1650 Orleans Street, Baltimore, Maryland 21231, USA
    Nat Genet 33:197-202. 2003
    ..We conclude that HIC1 is a candidate tumor-suppressor gene for which loss of function in both mouse and human cancers is associated only with epigenetic modifications...
  22. ncbi Reactive oxygen species: finding the right balance
    Craig N Morrell
    Circ Res 103:571-2. 2008

Research Grants3

  1. Nitric Oxide Regulation of Platelet Granule Exocytosis
    CRAIG MORRELL; Fiscal Year: 2007
    ..Therefore, strategies to minimize granule exocytosis may prove valuable in the acute treatment of pro-thrombotic diseases. (End of Abstract) ..