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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.