Annexin A10 contributes to chronic constrictive injury-induced pain through activating ERK1/2 signalling in rats. (1st February 2018)

• Record Type: Journal Article
• Authors: Li, Feng; Xue, Zhou-Ya; Liu, Xiang; Bai, Gang; Wang, Yuan-Lin
• Is Part Of: International journal of neuroscience. Volume 128:Number 2(2018)
• Page Start: 125
• Page End: 132
• Publication Date: 2018-02-01
• Subjects: Annexin A10 -- ERK1/2 -- TNF-α -- IL-1β -- pain; Nervous system -- Periodicals; 612.805
• DOI: 10.1080/00207454.2017.1375913
• Languages: English
• ISSNs: 0020-7454

Abstract

ABSTRACT: Purpose: The current study aims at investigating the downstream targets of spinal Annexin A10 in modulating neuropathic pain. Materials and methods: Paw withdrawal latency and paw withdrawal threshold were measured to evaluate the pain-associated behaviour in rats. The expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2 and extracellular regulated kinase were detected by western blotting. The level of tumour necrosis factor-α and interleukine-1β was tested by enzyme-linked immunosorbent assay (ELISA) kits. Results: Chronic constrictive injury caused pain hypersensitivity in rats, along with increased expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in rats. Knockdown of spinal Annexin A10 suppressed the chronic constrictive injury-induced hyperalgesia, and inhibited the chronic constrictive injury-induced increased expression of phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in the spinal cord. Inhibition of spinal extracellular regulated kinase activation decreased the release of tumour necrosis factor-α and interleukine-1β, but did not change the increased expression of Annexin A10 caused by chronic constrictive injury. Conclusions: Annexin A10 contributed to the development of neuropathic pain by activating spinal extracellular regulated kinase signalling and the subsequent release of tumour necrosis factor-α and interleukine-1β in the spinal cord.