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Articles, Neurobiology of Disease

The p38α MAPK Regulates Microglial Responsiveness to Diffuse Traumatic Brain Injury

Adam D. Bachstetter, Rachel K. Rowe, Machi Kaneko, Danielle Goulding, Jonathan Lifshitz and Linda J. Van Eldik
Journal of Neuroscience 3 April 2013, 33 (14) 6143-6153; DOI: https://doi.org/10.1523/JNEUROSCI.5399-12.2013
Adam D. Bachstetter
1Sanders-Brown Center on Aging,
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Rachel K. Rowe
2Department of Anatomy and Neurobiology, and
3Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536,
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Machi Kaneko
1Sanders-Brown Center on Aging,
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Danielle Goulding
1Sanders-Brown Center on Aging,
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Jonathan Lifshitz
4Barrow Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona 85004,
5Department of Child Health, University of Arizona College of Medicine, Phoenix, Arizona 85004, and
6Phoenix Veteran Affairs Healthcare System, Phoenix, Arizona 85004
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Linda J. Van Eldik
1Sanders-Brown Center on Aging,
2Department of Anatomy and Neurobiology, and
3Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536,
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Abstract

Neuropathology after traumatic brain injury (TBI) is the result of both the immediate impact injury and secondary injury mechanisms. Unresolved post-traumatic glial activation is a secondary injury mechanism that contributes to a chronic state of neuroinflammation in both animal models of TBI and human head injury patients. We recently demonstrated, using in vitro models, that p38α MAPK signaling in microglia is a key event in promoting cytokine production in response to diverse disease-relevant stressors and subsequent inflammatory neuronal dysfunction. From these findings, we hypothesized that the p38α signaling pathway in microglia could be contributing to the secondary neuropathologic sequelae after a diffuse TBI. Mice where microglia were p38α-deficient (p38α KO) were protected against TBI-induced motor deficits and synaptic protein loss. In wild-type (WT) mice, diffuse TBI produced microglia morphological activation that lasted for at least 7 d; however, p38α KO mice failed to activate this response. Unexpectedly, we found that the peak of the early, acute phase cytokine and chemokine levels was increased in injured p38α KO mice compared with injured WT mice. The increased cytokine levels in the p38α KO mice could not be accounted for by more infiltration of macrophages or neutrophils, or increased astrogliosis. By 7 d after injury, the cytokine and chemokine levels remained elevated in injured WT mice but not in p38α KO mice. Together, these data suggest that p38α balances the inflammatory response by acutely attenuating the early proinflammatory cytokine surge while perpetuating the chronic microglia activation after TBI.

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The Journal of Neuroscience: 33 (14)
Journal of Neuroscience
Vol. 33, Issue 14
3 Apr 2013
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The p38α MAPK Regulates Microglial Responsiveness to Diffuse Traumatic Brain Injury
Adam D. Bachstetter, Rachel K. Rowe, Machi Kaneko, Danielle Goulding, Jonathan Lifshitz, Linda J. Van Eldik
Journal of Neuroscience 3 April 2013, 33 (14) 6143-6153; DOI: 10.1523/JNEUROSCI.5399-12.2013

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The p38α MAPK Regulates Microglial Responsiveness to Diffuse Traumatic Brain Injury
Adam D. Bachstetter, Rachel K. Rowe, Machi Kaneko, Danielle Goulding, Jonathan Lifshitz, Linda J. Van Eldik
Journal of Neuroscience 3 April 2013, 33 (14) 6143-6153; DOI: 10.1523/JNEUROSCI.5399-12.2013
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