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Table 3 Differential gene expression of commonly dysregulated genes in experimental pain models

From: A comparison of RNA-seq and exon arrays for whole genome transcription profiling of the L5 spinal nerve transection model of neuropathic pain in the rat

Gene Symbol Gene name Fold change RNA-Seq Fold change exon arrays
Genes upregulated after SNT
Aif1/Iba-1 Allograft inflammatory factor 1 (Iba-1) 4.7 2.0
Apoe Apoliprotein E 1.5 (ns) 1.2
Arg1 Arginase, liver 30.1 2.4
Arpc1b Actin related protein 2/3 complex, subunit 1B, 41 kDa 3.7 2.7
Atf3 Activating transcription factor 3 33.8 13.7
C1qb Complement component 1, q subcomponent, B chain 10.1 5.5
C1qc Complement component 1, q subcomponent, C chain 7.7 4.5
C1s Complement component 1, s subcomponent 4.4 2.5
Cacna2d1 Calcium channel, voltage-dependent, alpha 2/delta subunit 1 5.0 3.0
Ccl2 Chemokine (C-C motif) ligand 2 2.1 1.4
Ccnd1 Cyclin D1 4.1 2.7
Cd74 CD74 molecule, major histocompatibility complex, class II invariant chain 6.5 2.8
Coro1a Coronin 1-A 1.0 (ns) 1.2 (ns)
Crabp2 Cellular retinoic acid-binding protein 2 3.1 2.1
Csrp3 Cysteine and glycine-rich protein 3 (cardiac LIM protein) 590.2 22.6
Ctsd Cathepsin D precursor 1.4 (ns) 1.3
Ctsh Cathepsin H 1.6 1.3 (ns)
Cxcl10 Chemokine (C-X-C motif) ligand 10 7.5 3.8
Cxcl13 Chemokine (C-X-C motif) ligand 13 4.0 2.2
Egr1 Early growth response 1 2.2 1.8
Gabra5 Gamma-aminobutyric acid (GABA) A receptor, alpha 5 2. 5 2.1
Gadd45a Growth arrest and DNA-damage-inducible, alpha 6.8 4.6
Gal Galanin/GMAP prepropeptide 46.3 13.5
Gap43 Growth associated protein 43 3.2 2.3
Gfap Glial fibrillary acidic protein 8.8 3.8
Gfra1 GDNF family receptor alpha 1 3.2 2.1
Igfbp3 Insulin-like growth factor binding protein 3 4.7 2.9
Igfbp6 Insulin-like growth factor binding protein 6 1.8 1.5
Lum Lumican 2.5 1.6
Npy Neuropeptide Y Not detected 7.8
Reg3b Regenerating islet-derived 3 beta 61.0 20.1
S100a4 S100 calcium binding protein A4 2.8 1.9
Sprr1a Small proline-rich protein 1A/cornifin-1 176.6 57.9
Stmn4 Stathmin-like 4 6.1 3.2
Timp1 TIMP metallopeptidase inhibitor 1 3.5 2.1
Vgf VGF nerve growth factor inducible 5.3 2.5
Vip Vasoactive intestinal peptide 138.1 5.4
Genes downregulated after SNT
Atp1b3* ATPase, Na+/K + transporting, beta 3 polypeptide 0.6 0.8
Calca* Calcitonin-related polypeptide alpha 0.3 0.4
Cd55 CD55 molecule, decay accelerating factor for complement 0.2 0.3
Chrna3 Cholinergic receptor, nicotinic, alpha 3 (neuronal) 0.1 0.1
Ckmt1 Creatine kinase, mitochondrial 1, ubiquitous 0.2 0.3
Gabbr1 Gamma-aminobutyric acid (GABA) B receptor, 1 0.8 0.8 (ns)
Grik1 Glutamate receptor, ionotropic, kainate 1 0.2 0.1
Htr3a 5-hydroxytryptamine (serotonin) receptor 3A, ionotropic 0.1 0.1
Kcnc2 Potassium voltage-gated channel, Shaw-related subfamily, member 2 0.3 0.5
Nefh Neurofilament, heavy polypeptide 0.3 0.4
Nefl Neurofilament, light polypeptide 0.2 0.5
Nefm Neurofilament, medium polypeptide 0.3 0.5
Nsf N-ethylmaleimide-sensitive factor 0.5 0.5
Rab3a RAB3A, member RAS oncogene family 0.3 0.4
Rgs4 Regulator of G-protein signaling 4 0.2 0.2
Scn11a Sodium channel, voltage-gated, type XI, alpha subunit 0.1 0.1
Snap25 Synaptosomal-associated protein, 25 kDa 0.3 0.6
Sst* Somatostatin 0.1 0.1
Sv2b Synaptic vesicle glycoprotein 2B 0.3 0.3
Tac1* Tachykinin, precursor 1 0.3 0.3
Vsnl1 Visinin-like 1 0.2 0.3
Ywhag Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma polypeptide 0.5 0.7
  1. The list of genes resulted from a meta-analysis study of microarray data of DRG and/or spinal cord tissue in inflammatory and neuropathic pain models [4]. Fold changes expressed as ratio SNT/naive in L5 DRGs. All fold changes are significant (p < 0.1, FDR) except if indicated by “ns” – non significant. The direction of fold change is consistent between the exon array and RNA-Seq dataset and largely coincides with the reported trends. Exceptions are genes marked with “*” Atp1b3, Calca, Sst, Tac1 which are listed as upregulated in the meta-analysis study but are significantly downregulated in our study. In support of our results, qPCR data reported by LaCroix-Fralish et al. [4] suggested that these genes are down regulated (albeit not significantly) in DRG tissue after chronic constriction injury. Also Npy expression is not detected in RNA-seq because there is a paralogous gene to Npy sharing 98% sequence homology. Therefore, reads aligning to Npy would be deemed as ambiguous and discarded from our analysis. Mapping to the Rn4 assembly of the rat genome (where paralogous genes are not annotated) reveals a 36.4 upregulation of Npy.