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Persistent Alterations in Microglial Enhancers in a Model of Chronic Pain

Research output: Contribution to journalArticlepeer-review

Franziska Denk, Megan Crow, Athanasios Didangelos, Douglas M. Lopes, Stephen B. McMahon

Original languageEnglish
Pages (from-to)1771–1781
JournalCell Reports
Issue number8
Early online date12 May 2016
Accepted/In press27 Apr 2016
E-pub ahead of print12 May 2016
Published24 May 2016


King's Authors


Chronic pain is a common and devastating condition that induces well-characterized changes in neurons and microglia. One major unanswered question is why these changes should persist long after the precipitating injury has healed. Here, we suggest that some of the longer-lasting consequences of nerve injury may be hidden in the epigenome. Cell sorting and sequencing techniques were used to characterize the spinal cord immune response in a mouse model of chronic neuropathic pain. Infiltration of peripheral myeloid cells was found to be absent, and RNA sequencing (RNA-seq) of central microglia revealed transient gene expression changes in response to nerve ligation. Conversely, examination of microglial enhancers revealed persistent, post-injury alterations in close proximity to transcriptionally regulated genes. Enhancers are regions of open chromatin that define a cell’s transcription factor binding profile. We hypothesize that changes at enhancers may constitute a mechanism by which painful experiences are recorded at a molecular level.

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