Expression of granulocyte colony-stimulating factor 3 receptor in the spinal dorsal horn following spinal nerve ligation-induced neuropathic pain

Zhang,Enji; Lee,Sunyeul; Yi,Min‑Hee; Nan,Yongshan; Xu,Yinshi; Shin,Nara; Ko,Youngkwon; Lee,Young  Ho; Lee,Wonhyung; Kim,Dong  Woon

doi:10.3892/mmr.2017.6853

Expression of granulocyte colony-stimulating factor 3 receptor in the spinal dorsal horn following spinal nerve ligation-induced neuropathic pain

Authors:
- Enji Zhang
- Sunyeul Lee
- Min‑Hee Yi
- Yongshan Nan
- Yinshi Xu
- Nara Shin
- Youngkwon Ko
- Young Ho Lee
- Wonhyung Lee
- Dong Woon Kim
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Affiliations: Department of Anatomy and Medical Science, Brain Research Institute, Chungnam National University School of Medicine, Daejeon 301‑747, Republic of Korea, Department of Anesthesia and Pain Medicine, Chungnam National University Hospital, Daejeon 301‑747, Republic of Korea, Department of Anesthesiology, Yanbian University Hospital, Yanbian, Jilin 133000, P.R. China
Published online on: June 23, 2017 https://doi.org/10.3892/mmr.2017.6853
Pages: 2009-2015
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

In previous studies that have profiled gene expression in patients with complex regional pain syndrome (CRPS), the expression of granulocyte colony-stimulating factor 3 receptor (G‑CSFR) was elevated, as were a number of pain‑associated genes. The present study determined the expression of G‑CSFR and the mechanisms by which it may affect hypersensitivity, focusing on the signal transducer and activator of transcription 3 (STAT3)/transient receptor potential cation channel subfamily V 1 (TRPV1) signaling pathway in particular, which is an important mediator of pain. Following L5 spinal nerve ligation (SNL) surgery, the protein and mRNA levels of G‑CSFR increased in the ipsilateral spinal dorsal horn when compared with the sham and/or contralateral control. Double immunofluorescence further demonstrated that G‑CSFR colocalized with TRPV1 and phosphorylated STAT in the neurons of the spinal dorsal horn. G‑CSF treatment led to an increase in G‑CSFR and TRPV1 expression and phosphorylation of STAT3. These results indicate that G‑CSF‑induced G‑CSFR expression may activate TRPV1 by promoting phosphorylation of STAT3. Collectively, the results suggest, for the first time, that the expression of G‑CSFR in neurons following peripheral nerve injury may be involved in the induction and maintenance of neuropathic pain through the STAT3 and TRPV1 signaling pathway.

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