Adhesion molecules on murine brain microvascular endothelial cells: expression and regulation of ICAM-1 and Lgp 55☆
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Cited by (150)
Inhibition of monocyte adhesion to brain-derived endothelial cells by dual functional RNA chimeras
2014, Molecular Therapy Nucleic AcidsCitation Excerpt :ICAM-1, also known as CD54, plays an important role in cell-cell adhesion, extravasation, and inflammatory response.7 Normally, ICAM-1 is expressed at low levels on brain endothelium and perivascular astrocytes, but its expression rises dramatically in pathological conditions such as ischemic stroke,8 brain trauma, multiple sclerosis (MS),9 experimental autoimmune encephalomyelitis (EAE),10 Alzheimer's disease,11 and inflammatory conditions in vitro.12 ICAM-1 facilitates migration of leukocytes into the brain and initiates adhesion of microglia to neurons, which causes neuronal injury and death under disease conditions.13,14
Immune Aspects of the Blood–Brain Barrier
2010, NeuroImmune BiologyCitation Excerpt :The source of these cytokines may be the vascular cells, nearby non-vascular cells, or leukocytes drawn to a site of inflammation or injury. Pro-inflammatory cytokines, such as interleukin 1(IL-1) or tumor necrosis factor-alpha (TNFα), induce or upregulate the expression of several groups of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial leukocyte adhesion molecule-1 (E-selectin, ELAM-1) [25, 26]. Interferon-gamma (IFN γ) similarly upregulates the expression of ICAM-1, in addition to major histocompatibility (MHC) class I and class II molecules, and the death receptor signaling molecules Fas and TRAIL [27, 28].
Regulation of cytokine signaling and T-cell recruitment in the aging mouse brain in response to central inflammatory challenge
2010, Brain, Behavior, and ImmunityCitation Excerpt :The present findings of an increase of Mmp 12 expression in the brain of aged mice after saline injections indicate that this transcript could be especially sensitive to CSF perturbations and/or could be increased in basal conditions contributing to the inflammatory state of the aging brain. TNF-α is a most potent inducer of ICAM-1 (Fabry et al., 1992) and the progressive age-related upregulation of ICAM-1 protein we observed in the brain, and in particular in cerebral endothelial and glial cells, after administration of this cytokine reflects, therefore, an age-dependent amplification of this effect. No age-related difference was here observed in the upregulation of Icam-1 transcript a few hours after TNF-α injection, and the age-dependent increase of ICAM-1 protein we observed at 48 h may, therefore, reflect a time course in this response and/or translational changes.
Soluble adhesion molecules and angiotensin-converting enzyme in dementia
2007, Neurobiology of Disease
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Supported by NIH grants NS24261, HL31944, HL14230 (Arteriosclerosis Center of Research) and by Veterans' Administration research funds.