• Heejin Jeong, Young-Ji Na, Kihwan Lee, Yong Ho Kim, Yunsin Lee, Minho Kang, Bao-Chun Jiang, Young Il Yeom, Long-Jun Wu, Yong-Jing Gao, Junhyong Kim, and Seog Bae Oh.
• aPain Cognitive Function Research Center, Seoul National University, Seoul, Republic of Korea bDental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, Republic of Korea cDepartment of Biology, University of Pennsylvania, Philadelphia, PA, USA dMedical Genomics Research Center, Korea Research Institute of Bioscience & Biotechnology, Daejeon, Korea eDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA fPain Research Laboratory, Institute of Nautical Medicine, Nantong University, Nantong, Jiangsu, China gDepartment of Computer and Information Science, University of Pennsylvania, Philadelphia, PA, USA hDepartment of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, Republic of Korea.
• Pain. 2016 Apr 1; 157 (4): 964-76.

AbstractMicroglial 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.

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