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Transcriptome profiling of dorsal root ganglia in a rat model of complex regional pain syndrome type-I reveals potential mechanisms involved in pain

Authors Yin C, Hu Q, Liu B, Tai Y, Zheng X, Li Y, Xiang X, Wang P, Liu B

Received 26 September 2018

Accepted for publication 27 February 2019

Published 12 April 2019 Volume 2019:12 Pages 1201—1216

DOI https://doi.org/10.2147/JPR.S188758

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Katherine Hanlon


Chengyu Yin,1,2,* Qimiao Hu,1,* Boyu Liu,1,* Yan Tai,3 Xiaoli Zheng,1 Yuanyuan Li,1 Xuaner Xiang,1 Ping Wang,4 Boyi Liu1

1Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, People’s Republic of China; 2College of Life Science, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China; 3Academy of Chinese Medicine Sciences, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China; 4Department of Pathology, School of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China

*These authors contributed equally to this work

Purpose: Complex regional pain syndrome type-I (CRPS-I) is a progressive and devastating pain condition, which remains clinically challenging. The mechanisms of CRPS-I still remain largely unknown. We aim to identify transcriptome profiles of genes relevant to pain mechanisms and major pathways involved in CRPS-I.
Methods: A rat model of chronic post-ischemia pain (CPIP) was established to mimic CRPS-I. RNA-sequencing (RNA-Seq) was used to profile transcriptome of L4-6 dorsal root ganglia (DRGs) of a rat model of CRPS-I.
Results: CPIP model rats developed persistent mechanical/thermal hyperalgesia in ipsilateral hind paw. RNA-Seq identified a total of 295 differentially expressed genes (DEGs), including 195 up- and 100 downregulated, in ipsilateral DRGs of CPIP rats compared with sham rats. The expression of several representative genes was confirmed by qPCR. Functional analysis of DEGs revealed that the most significant enriched biological processes of upregulated genes include response to lipopolysaccharide, inflammatory response and cytokine activity, which are all important mechanisms mediating pain. We further screened DEGs implicated in pain progress, genes enriched in small- to medium-sized sensory neurons and enriched in TRPV1-lineage nociceptors. By comparing our dataset with other published datasets of neuropathic or inflammatory pain models, we identified a core set of genes and pathways that extensively participate in CPIP and other neuropathic pain states.
Conclusion: Our study identified transcriptome gene changes in DRGs of an animal model of CRPS-I and could provide insights into identifying promising genes or pathways that can be potentially targeted to ameliorate CRPS-I.

Keywords: RNA-Seq, pain, CRPS-I, dorsal root ganglion, neuropathic pain
 

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