Strain specific variation in cytokine regulated ICAM-1 expression by rat brain-endothelial cells.

Linke, A; Antonopoulos, M; Davies, Daniel; Male, David

doi:10.1016/s0165-5728(99)00231-3

Cited by 4 publications

(1 citation statement)

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“…Proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL1β), and interferon-γ (IFN-γ) have been shown to strongly enhance endothelial ICAM-1 expression (Fabry et al, 1992). Accordingly, brain microvascular endothelial cells (BMVECs) from EAE-resistant rat strains have been reported to have significantly attenuated induction of ICAM-1 following TNF-α or IFN-γ stimulation (Linke et al, 2000). Furthermore BMVECs from MS patients express higher levels of ICAM-1 than normal control cells (Lou et al, 1997).…”

Section: Pivotal Role Of Endothelial Icam-1 During Leukocyte Migratiomentioning

confidence: 99%

Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

2005

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(1) The vasculature of the blood-brain barrier allows only comparatively few leukocytes to enter and survey the healthy central nervous system (CNS). However, during pathological CNS inflammation, the number of leukocytes adhering to and penetrating the CNS vasculature increases strongly. (2) Endothelial adhesion molecules do not only mediate firm adhesion of leukocyte to vascular beds but also trigger signaling cascades within the endothelial cell, which play a crucial role in modulating subsequent leukocyte diapedesis. (3) Signaling through endothelial intercellular adhesion molecule-1 (ICAM-1, CD54) has been shown to induce changes of the endothelial cytoskeleton, transcription, and interendothelial junctions, all of which may be important in modulating endothelial disposition to infiltrating leukocytes. Furthermore, a number of recent reports document that drugs interfering with endothelial ICAM-1 signaling, efficiently reduce leukocyte migration both in vitro and in animal models of CNS inflammation. (4) These approaches are novel in as much as they target vascular beds rather than the penetrating leukocytes. Since endothelial ICAM-1 signaling appears to differ between different vascular beds we propose that such compounds could potentially be used as exquisite drugs in the treatment of neuroinflammatory diseases.

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Section: Pivotal Role Of Endothelial Icam-1 During Leukocyte Migratiomentioning

confidence: 99%

Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

2005

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Genetic Regulation of Nerve Cell Death/Glial Activation and Protective Effects of Myelin Basic Protein Autoimmune Neurotrophin Production in Mechanically Induced Neurodegeneration

Piehl¹,

Lidman²,

Olsson³

2004

Early Indicators Early Treatments Neuroprotection in Multiple Sclerosis

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The adhesion molecule ICAM-1 and its regulation in relation with the blood–brain barrier

Diétrich

2002

Journal of Neuroimmunology

223

168

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Strain specific variation in cytokine regulated ICAM-1 expression by rat brain-endothelial cells.

Cited by 4 publications

References 20 publications

Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

Pharmacological Targeting of ICAM-1 Signaling in Brain Endothelial Cells: Potential for Treating Neuroinflammation

Genetic Regulation of Nerve Cell Death/Glial Activation and Protective Effects of Myelin Basic Protein Autoimmune Neurotrophin Production in Mechanically Induced Neurodegeneration

The adhesion molecule ICAM-1 and its regulation in relation with the blood–brain barrier

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