Expression of granulocyte colony-stimulating factor 3 receptor in the spinal dorsal horn following spinal nerve ligation-induced neuropathic pain
| Autor: | Dong Woon Kim, Nara Shin, Yongshan Nan, Min‑Hee Yi, Sun Yeul Lee, Enji Zhang, Young Ho Lee, Youngkwon Ko, Wonhyung Lee, Yinshi Xu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male STAT3 Transcription Factor Cancer Research medicine.medical_specialty Pathology Spinal Cord Dorsal Horn TRPV1 TRPV Cation Channels Biochemistry Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Internal medicine Gene expression Granulocyte Colony-Stimulating Factor Receptors Colony-Stimulating Factor Genetics Medicine Animals Phosphorylation Receptor STAT3 Molecular Biology Ligation neuropathic pain Neurons biology business.industry spinal cord Articles granulocyte colony-stimulating factor 3 030104 developmental biology Endocrinology granulocyte colony-stimulating factor 3 receptor Spinal Nerves Oncology Neuropathic pain Peripheral nerve injury STAT protein biology.protein Molecular Medicine Neuralgia Signal transduction business 030217 neurology & neurosurgery transient receptor potential cation channel subfamily V 1 |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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