Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 299, Issue -, Pages 130-138Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2016.09.009
Keywords
Focal cerebral ischemia; Regeneration; Neural stem cells; Neuroprotection; Neuroinflammation
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Funding
- Marga and Walter Boll-Stiftung [210-10-15]
- Koln Fortune Program/Faculty of Medicine, University of Cologne, Germany [190/2014, 339/2015]
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Osteopontin (OPN) is constitutively expressed in the brain and upregulated during neuroinflammation, e.g., focal cerebral ischemia. In OPN-deficient mice, microglia are deregulated after ischemia, but specific OPN-effects on microglia remain elusive. Primary microglia were cultured in the presence or absence of OPN. The survival of microglia under stress conditions was dose-dependently increased by OPN. Lipopolysaccharides (LPS)-induced release of nitric oxide (NO), TNF-alpha, and IL-6, as well as expression of inducible Nitric Oxide Synthase (iNOS), were attenuated by OPN. Data suggest that OPN modulates microglia function by shifting their inflammatory profile towards a neutral anti-inflammatory phenotype. (C) 2016 Elsevier B.V. All rights reserved.
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