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Role of phospholipase A2s and lipid mediators in secondary damage after spinal cord injury

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Abstract

Inflammation is considered to be an important contributor to secondary damage after spinal cord injury (SCI). This secondary damage leads to further exacerbation of tissue loss and functional impairments. The immune responses that are triggered by injury are complex and are mediated by a variety of factors that have both detrimental and beneficial effects. In this review, we focus on the diverse effects of the phospholipase A2 (PLA2) superfamily and the downstream pathways that generate a large number of bioactive lipid mediators, some of which have pro-inflammatory and demyelinating effects, whereas others have anti-inflammatory and pro-resolution properties. For each of these lipid mediators, we provide an overview followed by a discussion of their expression and role in SCI. Where appropriate, we have compared the latter with their role in other neurological conditions. The PLA2 pathway provides a number of targets for therapeutic intervention for the treatment of SCI and other neurological conditions.

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Acknowledgements

The authors thank Margaret Attiwell for her help with the illustrations.

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Correspondence to Samuel David.

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The work performed in the laboratory of S.D. was supported by grants from the Canadian Institutes of Health Research (CIHR) and the Wings for Life Spinal Cord Research Foundation. Work carried out in the laboratory of R.L.-V. is supported by grants from the Wings for Life Spinal Cord Research Foundation and a Marie-Curie International Reintegration grant and by funds from the Fondo de Investigación Sanitaria (TERCEL and CIBERNED) and Ministerio de Ciencia e Innovación of Spain (SAF2010-17851). A.D.G. is supported by a postdoctoral fellowship from the CIHR Neuroinflammation Training Program.

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David, S., Greenhalgh, A.D. & López-Vales, R. Role of phospholipase A2s and lipid mediators in secondary damage after spinal cord injury. Cell Tissue Res 349, 249–267 (2012). https://doi.org/10.1007/s00441-012-1430-8

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