A Novel Role for Sema3a in Neuroprotection from Injury Mediated by Activated Microglia.
From: Department of Clinical Neurosciences, Centre for Brain Repair, University of Cambridge, Forvie Site, Cambridge CB2 2PY, United Kingdom.
The Journal of neuroscience : the official journal of the Society for Neuroscience
- Publish Date: Feb 2006
- ISSN: 1529-2401
- Volume: 26
- Issue: 6
- Pages: 1730-8
- Medium: Internet
- Language: English
- Citation (JAMA): Majed Henry H, Chandran Siddharthan, Niclou Simone P, et al. A Novel Role for Sema3a in Neuroprotection from Injury Mediated by Activated Microglia.. J. Neurosci. Feb 2006;26:1730-8
Abstract
Microglia exist under physiological conditions in a resting state but become activated after neuronal injury. Recent studies have highlighted the reciprocal role of neurons in controlling both the number and activity of microglia. In this study, microglia derived from newborn rat cortices were cultured and activated by interferon-gamma (IFNgamma) treatment, then exposed to recombinant Sema3A or conditioned medium derived from stressed embryonic cortical neurons. We found that activation of microglia by IFNgamma induced differential upregulation of the semaphorin receptors Plexin-A1 and Neuropilin-1. This result was confirmed by Northern blotting, reverse transcription-PCR, and Western blotting. Furthermore, recombinant Sema3A induced apoptosis of microglia when added to the in vitro culture, and a similar result was obtained on activated microglia when Sema3A was produced by stressed neurons. Using an in vivo model of microglia activation by striatal injection of lipopolysaccharide demonstrated a corresponding upregulation of Plexin-A1 and Neuropilin-1 in activated microglia and enhanced production of Sema3A by stressed adult neurons. These results suggest a novel semaphorin-mediated mechanism of neuroprotection whereby stressed neurons can protect themselves from further damage by activated microglia.
Mesh Headings (Keywords): Animals, Animals, Newborn, Apoptosis, Cell Culture Techniques, Cell Death, Cell Line, Humans, Interferon Type II, Meninges, Microglia, Neurons, Neuroprotective Agents, Rats, Reverse Transcriptase Polymerase Chain Reaction, Semaphorin-3A, Transfection
Check for Full Text / PubMed Unique Identifier (PMID): 16467521
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.