Proteomic identification of altered cerebral proteins in the complex regional pain syndrome animal model.

Francis Sahngun Nahm,Pyung Bok Lee,Yong Chul Kim,Sang-Soep Nahm,Zee-Yong Park

doi:10.1155/2014/498410

Abstract

Background. Complex regional pain syndrome (CRPS) is a rare but debilitating pain disorder. Although the exact pathophysiology of CRPS is not fully understood, central and peripheral mechanisms might be involved in the development of this disorder. To reveal the central mechanism of CRPS, we conducted a proteomic analysis of rat cerebrum using the chronic postischemia pain (CPIP) model, a novel experimental model of CRPS. Materials and Methods. After generating the CPIP animal model, we performed a proteomic analysis of the rat cerebrum using a multidimensional protein identification technology, and screened the proteins differentially expressed between the CPIP and control groups. Results. A total of 155 proteins were differentially expressed between the CPIP and control groups: 125 increased and 30 decreased; expressions of proteins related to cell signaling, synaptic plasticity, regulation of cell proliferation, and cytoskeletal formation were increased in the CPIP group. However, proenkephalin A, cereblon, and neuroserpin were decreased in CPIP group. Conclusion. Altered expression of cerebral proteins in the CPIP model indicates cerebral involvement in the pathogenesis of CRPS. Further study is required to elucidate the roles of these proteins in the development and maintenance of CRPS.

Highlights

Complex regional pain syndrome (CRPS) is a rare but serious and painful disorder
Group A exhibited a significant decrease in the mechanical threshold compared to Group C after the chronic postischemia pain (CPIP) procedure (P < 0.01, Figure 2)
These findings suggest that both functional and structural changes may occur in the cerebrum of CPIP animals, and altered protein expression can be related to the development of CRPS

Summary

Introduction

Complex regional pain syndrome (CRPS) is a rare but serious and painful disorder. CRPS can occur following a minor injury, such as a sprain or even softtissue blunt trauma, severe intractable pain from CRPS can impair the quality of life. The exact pathophysiology of CRPS is not fully understood, several pathological mechanisms, including oxidative stress [2], neurogenic inflammation [3], and alteration in the autonomic nervous system [4, 5], are known to play some roles in its development. The spreading of symptoms and signs of CRPS from the initial site of presentation to another limb is a well-known phenomenon, which may be due to aberrant central regulation of neurogenic inflammation [11]. These findings highlight the contribution of a cortical pain mechanism in patients with CRPS.

Methods

Results

Conclusion