Abstract
Background: In the central nervous system, the role of LCN2 as a chemokine inducer has been previously reported. Results: Peripheral nerve injury increased LCN2 expression. Lcn2 deficiency attenuated pain hypersensitivity, microglial activation, and chemokine production. Chemokine expression and pain behavior were induced by LCN2. Conclusion: The LCN2-chemokine axis plays a critical role in the pathogenesis of neuropathic pain. Significance: LCN2 can be targeted for treatment of neuropathic pain. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.
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CITATION STYLE
Jeon, S., Jha, M. K., Ock, J., Seo, J., Jin, M., Cho, H., … Suk, K. (2013). Role of lipocalin-2-chemokine axis in the development of neuropathic pain following peripheral nerve injury. Journal of Biological Chemistry, 288(33), 24116–24127. https://doi.org/10.1074/jbc.M113.454140
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