C Iadecola

Summary

Affiliation: University of Minnesota
Country: USA

Publications

  1. ncbi Reduced susceptibility to ischemic brain injury and N-methyl-D-aspartate-mediated neurotoxicity in cyclooxygenase-2-deficient mice
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Proc Natl Acad Sci U S A 98:1294-9. 2001
  2. ncbi Cerebral ischemia and inflammation
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota, Minneapolis, Minnesota, USA
    Curr Opin Neurol 14:89-94. 2001
  3. ncbi Cyclooxygenase-2 immunoreactivity in the human brain following cerebral ischemia
    C Iadecola
    Department of Neurology, University of Minnesota Medical School, Minneapolis 55455, USA
    Acta Neuropathol 98:9-14. 1999
  4. ncbi SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein
    C Iadecola
    Department of Neurology, University of Minnesota, Minneapolis 55455, USA
    Nat Neurosci 2:157-61. 1999
  5. ncbi The transcription factor interferon regulatory factor 1 is expressed after cerebral ischemia and contributes to ischemic brain injury
    C Iadecola
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Exp Med 189:719-27. 1999
  6. ncbi Cyclooxygenase-1 participates in selected vasodilator responses of the cerebral circulation
    K Niwa
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota, USA
    Circ Res 88:600-8. 2001
  7. ncbi Cyclooxygenase-2 contributes to functional hyperemia in whisker-barrel cortex
    K Niwa
    Center for Clinical and Molecular Neurobiology, Departments of Neurology and Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    J Neurosci 20:763-70. 2000
  8. ncbi Gene-dosing effect and persistence of reduction in ischemic brain injury in mice lacking inducible nitric oxide synthase
    X Zhao
    Center for Clinical and Molecular Neurobiology, Departments of Neurology and Neuroscience, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Brain Res 872:215-8. 2000
  9. ncbi Increased susceptibility to ischemic brain injury in cyclooxygenase-1-deficient mice
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    J Cereb Blood Flow Metab 21:1436-41. 2001
  10. ncbi Inducible nitric oxide synthase gene expression in vascular cells after transient focal cerebral ischemia
    C Iadecola
    Department of Neurology, University of Minnesota Medical School Minneapolis 55455, USA
    Stroke 27:1373-80. 1996

Detail Information

Publications21

  1. ncbi Reduced susceptibility to ischemic brain injury and N-methyl-D-aspartate-mediated neurotoxicity in cyclooxygenase-2-deficient mice
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Proc Natl Acad Sci U S A 98:1294-9. 2001
    ..Thus, COX-2 is involved in pathogenic events occurring in both the early and late stages of cerebral ischemia and may be a valuable therapeutic target for treatment of human stroke...
  2. ncbi Cerebral ischemia and inflammation
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota, Minneapolis, Minnesota, USA
    Curr Opin Neurol 14:89-94. 2001
    ..Therefore, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia...
  3. ncbi Cyclooxygenase-2 immunoreactivity in the human brain following cerebral ischemia
    C Iadecola
    Department of Neurology, University of Minnesota Medical School, Minneapolis 55455, USA
    Acta Neuropathol 98:9-14. 1999
    ..The data suggest that COX-2 up-regulation is also relevant to cerebral ischemia in humans and raise the possibility that COX-2 reaction products participate in the mechanisms of ischemic injury also in the human brain...
  4. ncbi SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein
    C Iadecola
    Department of Neurology, University of Minnesota, Minneapolis 55455, USA
    Nat Neurosci 2:157-61. 1999
    ..These cerebrovascular effects of peptides derived from APP processing may contribute to the alterations in cerebral blood flow and to neuronal dysfunction in Alzheimer's dementia...
  5. ncbi The transcription factor interferon regulatory factor 1 is expressed after cerebral ischemia and contributes to ischemic brain injury
    C Iadecola
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Exp Med 189:719-27. 1999
    ..Thus, IRF-1 is the first nuclear transacting factor demonstrated to contribute directly to cerebral ischemic damage and may be a novel therapeutic target in ischemic stroke...
  6. ncbi Cyclooxygenase-1 participates in selected vasodilator responses of the cerebral circulation
    K Niwa
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota, USA
    Circ Res 88:600-8. 2001
    ..The data provide evidence for a critical role of COX-1 in maintaining resting vascular tone and in selected vasodilator responses of the cerebral microcirculation...
  7. ncbi Cyclooxygenase-2 contributes to functional hyperemia in whisker-barrel cortex
    K Niwa
    Center for Clinical and Molecular Neurobiology, Departments of Neurology and Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    J Neurosci 20:763-70. 2000
    ..The findings provide evidence for a previously unrecognized role of COX-2 in the mechanisms coupling synaptic activity to neocortical blood flow and provide an insight into one of the functions of constitutive COX-2 in the CNS...
  8. ncbi Gene-dosing effect and persistence of reduction in ischemic brain injury in mice lacking inducible nitric oxide synthase
    X Zhao
    Center for Clinical and Molecular Neurobiology, Departments of Neurology and Neuroscience, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Brain Res 872:215-8. 2000
    ..We conclude that the reduction in ischemic damage conferred by iNOS deletion exhibits a gene-dosing effect and that the protection is long lasting...
  9. ncbi Increased susceptibility to ischemic brain injury in cyclooxygenase-1-deficient mice
    C Iadecola
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    J Cereb Blood Flow Metab 21:1436-41. 2001
    ..Thus, the vascular effects of COX-1 may contribute to maintain cerebral blood flow in the postischemic brain and, as such, play a protective role in ischemic brain injury...
  10. ncbi Inducible nitric oxide synthase gene expression in vascular cells after transient focal cerebral ischemia
    C Iadecola
    Department of Neurology, University of Minnesota Medical School Minneapolis 55455, USA
    Stroke 27:1373-80. 1996
    ....
  11. ncbi Cyclooxygenase-2 inhibitor ns-398 protects neuronal cultures from lipopolysaccharide-induced neurotoxicity
    E Araki
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota, Minneapolis 55455, USA
    Stroke 32:2370-5. 2001
    ..The data support the hypothesis that COX-2, in addition to its role in glutamate excitotoxicity, participates in the cytotoxicity associated with inflammation...
  12. ncbi A beta-peptides enhance vasoconstriction in cerebral circulation
    K Niwa
    Center for Clinical and Molecular Neurobiology, Department of Neurology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Am J Physiol Heart Circ Physiol 281:H2417-24. 2001
    ..The vascular actions of A beta may contribute to the deleterious effects resulting from accumulation of this peptide in Alzheimer's dementia...
  13. ncbi Stellate neurons mediate functional hyperemia in the cerebellar molecular layer
    G Yang
    Center for Clinical and Molecular Neurobiology, Department of Neurology, School of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Neurosci 20:6968-73. 2000
    ..The data provide evidence that stellate neurons are a critical link between neural activity and blood flow in the activated cerebellum and that NO is the principal effector of their vascular actions...
  14. ncbi The cyclooxygenase-2 inhibitor NS-398 ameliorates ischemic brain injury in wild-type mice but not in mice with deletion of the inducible nitric oxide synthase gene
    M Nagayama
    Department of Neurology, University of Minnesota Medical School, Minneapolis, USA
    J Cereb Blood Flow Metab 19:1213-9. 1999
    ..Thus, COX-2 reaction products may be another mechanism by which iNOS-derived NO contributes to ischemic brain injury...
  15. ncbi Delayed reduction of ischemic brain injury and neurological deficits in mice lacking the inducible nitric oxide synthase gene
    C Iadecola
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Neurosci 17:9157-64. 1997
    ..iNOS inhibition may provide a novel therapeutic strategy targeted specifically at the secondary progression of ischemic brain injury...
  16. ncbi Effect of hyperoxia, hypercapnia, and hypoxia on cerebral interstitial oxygen tension and cerebral blood flow
    T Q Duong
    Department of Radiology, Center for Magnetic Resonance Research, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455, USA
    Magn Reson Med 45:61-70. 2001
    ..This methodology may prove useful for investigating cerebral piO(2) under pathologically or functionally altered conditions. Magn Reson Med 45:61-70, 2001...
  17. ncbi Molecular pathology of cerebral ischemia: delayed gene expression and strategies for neuroprotection
    C Iadecola
    Department of Neurology, University of Minnesota Medical School, Minneapolis 55455, USA
    Ann N Y Acad Sci 835:203-17. 1997
    ..Inhibition of iNOS or COX-2 offers the prospect of treatments directed to the late stages of the damage. However, additional preclinical studies would be necessary before these new treatment strategies can be tested in human stroke...
  18. ncbi Susceptibility to cell death induced by mutant SV40 T-antigen correlates with Purkinje neuron functional development
    R M Feddersen
    Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis 55455, USA
    Mol Cell Neurosci 9:42-62. 1997
    ..These data indicate that Purkinje cell death susceptibility varies with developmental stage...
  19. ncbi Relative changes of cerebral arterial and venous blood volumes during increased cerebral blood flow: implications for BOLD fMRI
    S P Lee
    Center for Magnetic Resonance Research, Department of Radiology, University of Minnesota Medical School, Minneapolis 55455, USA
    Magn Reson Med 45:791-800. 2001
    ..The absolute venous blood volume change contributes up to 36% of the total blood volume change during hypercapnia. Our findings provide a quantitative physiological model of BOLD contrast...
  20. ncbi Angiotensin II AT-1A receptor immunolabeling in rat medial nucleus tractus solitarius neurons: subcellular targeting and relationships with catecholamines
    M J Glass
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 East 69th Street, New York, NY 10021, USA
    Neuroscience 130:713-23. 2005
    ..These results suggest that AT-1A receptors are positioned for modulation of catecholamine signaling in the mNTS...
  21. ncbi The neurovascular dysfunction induced by angiotensin II in the mouse neocortex is sexually dimorphic
    H Girouard
    Division of Neurobiology, Weill Cornell Medical College, 411 E 69th Street, New York, NY 10021, USA
    Am J Physiol Heart Circ Physiol 294:H156-63. 2008
    ..Such protection from the deleterious cerebrovascular effects of hypertension may play a role in the reduced vulnerability to the cerebrovascular complications of hypertension observed in women...