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