Year: 2016
Type: article
Abstract: 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.
Source: Cell Reports
Institutions: King's College London, Cold Spring Harbor Laboratory
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $5,620
Awards: Identifying novel pain mediators and mechanisms., ERA-NET NEURON: Identification and study of different immune cell populations and their role in chronic pain, G5726110920, G5846212695, Understanding the genetic basis of common human diseases: core funding for the Wellcome Trust Centre for Human Genetics., Identifying Novel Pain Mediators and Mechanisms., Understanding the genetic basis of common human diseases: core funding for the Wellcome Trust Centre for Human Genetics., G8975541179
OpenAlex ID: W2369050436