title: Comparison of gene expression profiles in neuropathic and inflammatory pain.
abstract: Molecular mechanisms underlying the differences between chronic neuropathic and inflammatory pain are still poorly understood. Identifying those differences should provide insight into the molecular mechanism underlying features unique for neuropathic pain, such as allodynia. We have performed screening for differentially expressed genes in the spinal cord in the rat models of neuropathic and inflammatory pain. Using BD Atlas Rat 4K arrays we found several differences in expression of secretion-related genes between inflammatory and neuropathic pain. Development of the latter was characterized by up-regulated expression of genes associated with immune response and microglia activation and also, to a lesser extent, with cytoskeleton rearrangement. The relative increase in abundance of four genes, intercellular adhesion molecule 1 (ICAM-1), calcitonin gene related peptide (CGRP), tissue inhibitor of metalloproteinase 1 (TIMP-1), chemokine-like receptor 1 was confirmed by reverse transcription Real-Time PCR (qPCR) validation in the spinal cord in neuropathic pain. Levels of transcripts corresponding to ICAM-1 and TIMP-1 were also increased in the dorsal root ganglia (DRG) of neuropathic rats. Our data point at the importance of immune response- and microglia activation-related genes in the development of chronic neuropathic pain, and suggest that expression of CGRP gene in the dorsal horn of the spinal cord could be involved in persistence of its symptoms.
authors.affiliation: Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, 31-343 Krakow, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Rodriguez Parkitna
authors.forename: M
authors.initials: M
authors.lastname: Korostynski
authors.forename: D
authors.initials: D
authors.lastname: Kaminska-Chowaniec
authors.forename: I
authors.initials: I
authors.lastname: Obara
authors.forename: J
authors.initials: J
authors.lastname: Mika
authors.forename: B
authors.initials: B
authors.lastname: Przewlocka
authors.forename: R
authors.initials: R
authors.lastname: Przewlocki
mesh_terms: D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation; D005620:Freund's Adjuvant; D005727:Ganglia, Spinal / Q000276:immunology; D020869:Gene Expression Profiling; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D017628:Microglia / Q000378:metabolism; D023421:Models, Animal; D008969:Molecular Sequence Data; D009437:Neuralgia / Q000235:genetics / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D010146:Pain / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism; D012584:Sciatic Nerve / Q000293:injuries / Q000378:metabolism; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
chemical_list: C109811:Cmklr1 protein, rat; D008565:Membrane Proteins; D019707:Receptors, Chemokine; D019715:Tissue Inhibitor of Metalloproteinase-1; D018799:Intercellular Adhesion Molecule-1; D005620:Freund's Adjuvant; D015740:Calcitonin Gene-Related Peptide