Pyung-Bok Lee, Young Hoon Kim, Eunjoo Choi and Francis Sahngun Nahm
Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
Posters & Accepted Abstracts: J Pharmacogenomics Pharmacoproteomics
Background & Aim: Complex regional pain syndrome (CRPS) is a rare but debilitating pain disorder. Although the exact pathophysiology of COPS is not fully understood, central and peripheral mechanism 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 (CIPI) model, a novel experimental model of CRPS. Materials & 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. Based on these findings, we conducted confirmation study and determined calmodulin (CaM) and Ca2+/CaM kinase II (CaMKII) protein expression by Western blotting. 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. The expression of CaM (P=0.058), cereblon (P=0.007) and neuroserpin (P=0.070) 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.
Email: painfree@snubh.org