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Published on: September 7, 2019
High-resolution transcriptome analysis reveals neuropathic pain gene-expression signatures in spinal microglia after
Heejin Jeong1, Young-Ji Na, Kihwan Lee
1Pain Cognitive Function Research Center, Seoul National University, Seoul, Republic of Korea Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea Department of Biology, University of Pennsylvania, Philadelphia, PA, USA Medical Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology, Daejeon, Korea Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA Pain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong, Jiangsu, China Department of Computer and Information Science, University of Pennsylvania, Philadelphia, PA, USA Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea.
Abstract:
Microglial cells, the resident immune cells of the spinal cord, become activated in response to peripheral nerve injury. Microglia activation contributes to the development of neuropathic pain. Here we employed microarray analysis of individually collected pools of 10 spinal microglia cells to identify changes of levels and cell-to-cell expression variance of microglial genes during their activation after peripheral nerve injury. The analysis of microglia on postoperative day 1 (POD1) identified miR-29c as a critical factor for microglial activation and the development of neuropathic pain. Early POD1 microglia exhibited a very distinct expression profile compared to late POD7 microglia, possibly leading to the transition from initiation to maintenance of neuropathic pain. We found sample variance patterns that were consistent with the hypothesis that microglia were highly heterogeneous at the level of individual cells, and variation analysis identified 56 microglial genes potentially linked to the maintenance of neuropathic pain which included Gria1. This study provides insights into spinal microglial biology and reveals novel microglial targets for the treatment of neuropathic pain.
Insights
Spinal microglia activation after nerve injury drives neuropathic pain. Researchers identified miR-29c and 56 other genes, including Gria1, as key players in pain development and maintenance, offering new therapeutic targets.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Microglial cells in the spinal cord are immune cells that activate following peripheral nerve injury.
- Microglia activation is a key factor in the development of neuropathic pain.
Purpose of the Study:
- To identify gene expression changes and cell-to-cell variance in spinal microglia during activation after peripheral nerve injury.
- To uncover novel molecular targets for treating neuropathic pain.
Main Methods:
- Microarray analysis was performed on individually collected pools of 10 spinal microglia cells.
- Gene expression profiles were analyzed at postoperative day 1 (POD1) and POD7.
Main Results:
- Microglia activation on POD1 identified miR-29c as critical for neuropathic pain development.
- Distinct expression profiles between early (POD1) and late (POD7) microglia suggest roles in pain initiation versus maintenance.
- Variation analysis identified 56 microglial genes, including Gria1, potentially involved in maintaining neuropathic pain, highlighting significant cellular heterogeneity.
Conclusions:
- Spinal microglia exhibit significant heterogeneity, with distinct profiles correlating with different stages of neuropathic pain.
- miR-29c and other identified genes represent potential therapeutic targets for neuropathic pain management.
