Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 181, Issue 3, Pages 978-992Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2012.06.007
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Funding
- National Health and Medical Research Council of Australia [454723]
- Career Development Award Fellowship
- Transport Accident Commission
- NIH [1R43CA132395-01A2]
- Victorian State Government's Department of Innovation, Industry, and Regional Development
- Australian government (AusAID)
- State Government of Victoria
- Australian government
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Evidence suggests a proinflammatory role of lysophosphatidic acid (LPA) in various pathologic abnormalities, including in the central nervous system. Herein, we describe LPA as an important mediator of inflammation after spinal cord injury (SCI) in zebrafish and mice. Furthermore, we describe a novel monoclonal blocking antibody raised against LPA that potently inhibits LPA's effect in vitro and in vivo. This antibody, B3, specifically binds LPA, prevents it from interacting with its complement of receptors, and blocks LPA's effects on the neuronal differentiation of human neural stem/progenitor cells, demonstrating its specificity toward LPA signaling. When administered systemically to mice subjected to SCI, B3 substantially reduced glial inflammation and neuronal death. B3-treated animals demonstrated significantly more neuronal survival upstream of the lesion site, with some functional improvement. This study describes the use of anti-LPA monoclonal antibody as a novel therapeutic approach for the treatment of SCI. (Am J Pathol 2012, 181:978-992; http://dx.doi.org/10.1016/j.ajpath.2012.06.007)
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