Catestatin Enhances Neuropathic Pain Mediated by P2X4 Receptor of Dorsal Root Ganglia in a Rat Model of Chronic Constriction Injury

Autor: Huiyu Chen, Qiqing He, Changshui Xu, Errong Du, Zeyu Deng, Bihan Xia, Congcong Li, Chenglong Liu
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
Physiology
Neuropathic pain
p38 Mitogen-Activated Protein Kinases
lcsh:Physiology
Rats
Sprague-Dawley

Pathogenesis
0302 clinical medicine
Ganglia
Spinal

lcsh:QD415-436
RNA
Small Interfering

Receptor
Dorsal root ganglia
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Behavior
Animal

medicine.diagnostic_test
Glial fibrillary acidic protein
biology
lcsh:QP1-981
Nuclear factor-κB
Constriction
Up-Regulation
medicine.anatomical_structure
Hyperalgesia
RNA Interference
medicine.symptom
Catestatin
medicine.medical_specialty
Central nervous system
lcsh:Biochemistry
03 medical and health sciences
Western blot
Downregulation and upregulation
Internal medicine
Glial Fibrillary Acidic Protein
medicine
Animals
Tumor Necrosis Factor-alpha
business.industry
Transcription Factor RelA
Mitogenactivated protein kinase
Peptide Fragments
Rats
Disease Models
Animal

030104 developmental biology
Endocrinology
Proinfammatory cytokines
biology.protein
Chromogranin A
Neuralgia
Satellite glial cells
business
Receptors
Purinergic P2X4

human activities
P2X4 receptor
030217 neurology & neurosurgery
Zdroj: Cellular Physiology and Biochemistry, Vol 51, Iss 2, Pp 812-826 (2018)
ISSN: 1421-9778
1015-8987
Popis: Background/Aims: Neuropathic pain (NPP) is the consequence of a number of central nervous system injuries or diseases. Previous studies have shown that NPP is mediated by P2X4 receptors that are expressed on satellite glial cells (SGCs) of dorsal root ganglia (DRG). Catestatin (CST), a neuroendocrine multifunctional peptide, may be involved in the pathogenesis of NPP. Here, we studied the mechanism through which CST affects NPP. Methods: We made rat models of chronic constriction injury (CCI) that simulate neuropathic pain. Rat behavioral changes were estimated by measuring the degree of hyperalgesia as assessed by the mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL). P2X4 mRNA expression was detected by quantitative real-time reverse transcription-polymerase chain reaction. P2X4 protein level and related signal pathways were assessed by western blot. Additionally, double-labeled immunofluorescence was employed to visualize the correspondence between the P2X4 receptor and glial fibrillary acidic protein. An enzyme-linked immunosorbent assay was performed to determine the concentration of CST and inflammatory factors. Results: CST led to lower MWT and TWL and increased P2X4 mRNA and protein expression on the SGCs of model rats. Further, CST upregulated the expression of phosphor-p38 and phosphor-ERK 1/2 on the SGCs of CCI rats. However, the expression level of phosphor-JNK and phosphor-p65 did not obviously change. Conclusion: Taken together, CST might boost NPP by enhancing the sensitivity of P2X4 receptors in the DRG of rats, which would provide us a novel perspective and research direction to explore new therapeutic targets for NPP.
Databáze: OpenAIRE