Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts

  • Authors:
    • Koji Fukuda
    • Yasushi Miura
    • Toshihisa Maeda
    • Masayasu Takahashi
    • Shinya Hayashi
    • Masahiro Kurosaka
  • View Affiliations

  • Published online on: August 1, 2013     https://doi.org/10.3892/ijmm.2013.1461
  • Pages: 910-916
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Abstract

Decoy receptor 3 (DcR3), a member of the tumor necrosis factor (TNF) receptor (TNFR) superfamily, lacks the transmembrane domain of conventional TNFRs in order to be a secreted protein. DcR3 competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT and TNF-like ligand 1A (TL1A). We previously reported that TNFα-induced DcR3 overexpression in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) protects cells from Fas-induced apoptosis. Previous studies have suggested that DcR3 acting as a ligand directly induces the differentiation of macrophages into osteoclasts. Furthermore, we reported that DcR3 induces very late antigen-4 (VLA-­4) expression in THP-1 macrophages, inhibiting cycloheximide-induced apoptosis and that DcR3 binds to membrane-bound TL1A expressed on RA-FLS, resulting in the negative regulation of cell proliferation induced by inflammatory cytokines. In the current study, we used cDNA microarray to search for genes in RA-FLS whose expression was regulated by the ligation of DcR3. The experiments revealed the expression profiles of genes in RA-FLS regulated by DcR3. The profiles showed that among the 100 genes most significantly regulated by DcR3, 45 were upregulated and 55 were downregulated. The upregulated genes were associated with protein complex assembly, cell motility, regulation of transcription, cellular protein catabolic processes, cell membrane, nucleotide binding and glycosylation. The downregulated genes were associated with transcription regulator activity, RNA biosynthetic processes, cytoskeleton, zinc finger region, protein complex assembly, phosphate metabolic processes, mitochondrion, ion transport, nucleotide binding and cell fractionation. Further study of the genes detected in the current study may provide insight into the pathogenesis and treatment of rheumatoid arthritis by DcR3-TL1A signaling.

Introduction

Rheumatoid arthritis (RA) is an inflammatory joint disease characterized by hyperplasia of the synovial tissue and formation of pannus, which grows invasively into the cartilage, causing cartilage and bone destruction. Analyses of hyperplastic synovial tissue of patients with RA have revealed a number of features of transformed long-living cells, such as the presence of somatic mutations, expression of oncogenes and resistance to apoptosis (13).

We previously reported that the decoy receptor 3 (DcR3)/TR6/M68/tumor necrosis factor receptor (TNFR) superfamily member 6 (TNFRSF6b) is expressed in rheumatoid fibroblast-like synoviocytes (RA-FLS), and that DcR3 expression induced in RA-FLS by TNFα protects cells from Fas-induced apoptosis (4). DcR3, a member of the TNFR superfamily, lacks the transmembrane domain of conventional TNFRs and thus can be a secreted protein (5). DcR3 is typically overexpressed in tumor cells, including lung and colon cancers (5), gliomas, gastrointestinal tract tumors (6) and virus-associated leukemia (7). In addition, as previous studies have demonstrated, DcR3 is expressed in some normal tissues, including the colon, stomach, spleen, lymph nodes, spinal cord, pancreas and lungs (5,6). However, DcR3 is not expressed in NIH3T3 human fibroblast cells (8). DcR3 has 3 ligands, Fas ligand (FasL), LIGHT and TNF-like ligand 1A (TL1A), which are members of the TNF superfamily (9). The overexpression of DcR3 may benefit tumors by helping them avoid the cytotoxic and regulatory effects of FasL (5,10), LIGHT (11) and TL1A (12). In a previous study, we suggested that DcR3 is one of the key molecules that regulate the proliferation of RA-FLS (4).

Previous studies have suggested that DcR3 directly induces osteoclast formation from monocytes (13), and that DcR3 triggers the enhanced adhesion of monocytes via reverse signaling (14). We have also reported that DcR3 induces very late antigen-4 (VLA-4) expression in THP-1 macrophages, inhibiting cycloheximide-induced apoptosis (15). As for RA-FLS, in a recent study, we reported that DcR3 binds to membrane-bound TL1A expressed on RA-FLS, resulting in the negative regulation of cell proliferation induced by inflammatory cytokines (16). Therefore, we hypothesized that DcR3 plays a role in the pathogenesis of RA, not only as a decoy receptor, but also as a ligand via TL1A on RA-FLS. However, the function of DcR3 as a ligand in RA-FLS is not yet well understood. In the current study, we searched for genes in RA-FLS whose expression was regulated by the ligation of DcR3 using cDNA microarray. The gene expression profiles may reveal the possible target molecules that play a significant role in the DcR3-TL1A signaling pathway in the pathogenesis of RA.

Materials and methods

Isolation and culture of synovial fibroblasts

RA-FLS were obtained during total knee replacement surgery from 4 patients (samples 1–4) with RA who fulfilled the 1987 criteria of the American College of Rheumatology (formerly, the American Rheumatism Association) (17), who had never been treated with biological drugs. Synovial samples were collected from the patients who provided written consent in order to participate in this study in accordance with the World Medical Association Declaration of Helsinki Ethical Principles for Medical Research Involving Human Subjects. The protocol, including consent procedures, was approved by Kobe University Graduate School of Medicine Ethics Committee. Tissue specimens were minced and digested in Dulbecco’s modified Eagle’s medium (DMEM; Gibco BRL, Grand Island, NY, USA) containing 0.2% collagenase (Sigma, St. Louis, MO, USA) for 2 h at 37°C with 5% CO2. The dissociated cells were cultured in DMEM supplemented with 10% fetal bovine serum (FBS; BioWhittaker, Walkersville, MD, USA) and 100 U/ml of penicillin/streptomycin. Following overnight culture, the non-adherent cells were removed, and the adherent cells were subsequently incubated further in fresh medium. All experiments were conducted using cells from passages 3 to 4 (4).

RNA extraction

Four individual lines (samples 1–4) of primary cultured RA-FLS (2×106 cells/well) were incubated with 1.0 μg/ml of recombinant DcR3-Fc protein or control human IgG1 (R&D Systems, Minneapolis, MN, USA) for 12 h at 37°C with 5% CO2. Following incubation, RNA was extracted using a QIAshredder and the RNeasy Mini kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. Extraction of total RNA was performed for each sample separately.

Gene expression profiling and data analysis

Gene expression was detected by microarray (Human Genome U133 Plus 2.0, GeneChip® 3′ Expression Array; Affymetrix, Santa Clara, CA, USA). The labeling of RNA probes, hybridization and washing were carried out according to the manufacturer’s instructions.

Avadis 3.3 Prophetic software (Strand Life Sciences, Bangalore, India) was used for statistical analysis. Differentially expressed genes were extracted by a paired t-test, with a P-value <0.05 considered to indicate a statistically significant difference, and fold change >1.4, and ordered into hierarchical clusters using the Euclidean algorithm as the distance measure, and the complete algorithm as the linkage method.

Microarray data have been deposited in NCBIs Gene Expression Omnibus (GEO) and are accessible through GEO series accession no. GSE45665.

Results

Microarray analysis (gene expression profiling of RA-FLS stimulated by DcR3-Fc)

Microarray data analysis revealed that DcR3 upregulated or downregulated the expression of various genes in RA-FLS. We identified the 100 most differentially regulated genes in the DcR3-stimulated group compared with the control IgG1-stimulated group. Among these, 45 genes were upregulated (Table I) and 55 genes were downregulated (Table II).

Table I

The 45 genes upregulated by DcR3.

Table I

The 45 genes upregulated by DcR3.

Gene symbolRepresentative public IDP-valueFold changeGene title
---AW6124610.0026954432.0972981---
CDH2NM_0017920.03272611.9276143Cadherin 2, type 1, N-cadherin (neuronal)
AGPAT9BC0062360.0067821951.9184313 1-Acylglycerol-3-phosphate O-acyltransferase 9
LOC440944BC0366980.0394327831.8932389Hypothetical protein LOC440944
BIVMBC0395870.0127606831.6798534Basic, immunoglobulin-like variable motif-containing protein
ZC3H3D634840.029146551.6767992Zinc finger CCCH-type containing 3
IL12BNM_0021870.0083061351.6463093Interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40)
NUB1AK0264330.0458518271.6456505Negative regulator of ubiquitin-like proteins 1
LTV1AW2362140.0024769141.6453595LTV1 homolog (S. cerevisiae)
DMRT2AF2842250.0335027461.6123677Doublesex and mab-3 related transcription factor 2
SUZ12PAI8207960.0215935631.5686668Suppressor of zeste 12 homolog pseudogene
ZBTB1BU9503800.0397868641.5227357Zinc finger and BTB domain containing 1
---N297160.002775711.5223095---
---AK0907620.0344674661.5185958---
---BG3989770.0150837931.5135463---
RANBP17NM_0228970.0215182661.5035642RAN binding protein 17
GAS5BF3369360.0413669571.499078Growth arrest-specific 5 (non-protein coding)
---BC0319960.0112586531.4903411---
REPS2AI9846070.0121210661.4882914RALBP1 associated Eps domain containing 2
LOC645158BC0180880.0139217991.4854323Hypothetical protein LOC645158
---AI3324540.0126770741.4752275---
CCDC138AU1529650.0225188231.4711432Coiled-coil domain containing 138
hCG_1749898BC0124860.0022762731.471024KRTAPx protein
---AI6932810.01965661.4607961---
TUBB2BAL5338380.0066284091.4584572Tubulin, beta 2B
SLC9A9AA0297910.0042986571.4567653Solute carrier family 9 (sodium/hydrogen exchanger), member 9
---AA5051350.0234161781.4560933---
SLC16A6AI8732730.0321263371.4534916Solute carrier family 16, member 6 (monocarboxylic acid transporter 7)
---AL0801120.0356478281.4486992---
LOC100128988AI7614360.0359676851.4464797Similar to hCG2018847
ZNF252AU1456620.0157984161.4447424Zinc finger protein 252
FGFR1OP2R917660.0219767911.4398756FGFR1 oncogene partner 2
---R269310.039319691.4398652---
ZBTB10BG4838020.0061686981.4324573Zinc finger and BTB domain containing 10
C3AR1U620270.0316169671.4275972Complement component 3a receptor 1
ZER1NM_0063360.0005299481.4270489Zer-1 homolog (C. elegans)
THRBBF4319890.0270432251.4229552Thyroid hormone receptor, beta (erythroblastic leukemia viral (v-erb-a) oncogene homolog 2, avian)
FLJ35220AI3110400.0082029071.422941Hypothetical protein FLJ35220
CDH10NM_0067270.0188719331.4211183Cadherin 10, type 2 (T2-cadherin)
PEX13BC0409530.006700111.4182297Peroxisomal biogenesis factor 13
C7orf58NM_0249130.044626391.4087468Chromosome 7 open reading frame 58
DOK3BC0045640.0398093461.4068991Docking protein 3
---CA7765050.0388756841.4046313---
EGR3NM_0044300.0086573681.4038599Early growth response 3
ZNF681BG2819400.0092792831.4019198Zinc finger protein 681

[i] DcR3, decoy receptor 3.

Table II

The 55 genes downregulated by DcR3.

Table II

The 55 genes downregulated by DcR3.

Gene symbolRepresentative public IDP-valueFold changeGene title
TPH1NM_0041790.0223983732.4520018Tryptophan hydroxylase 1
TREML4AK0906330.0285594391.9765018Triggering receptor expressed on myeloid cells-like 4
CEP70AI2858840.0387452131.8690827Centrosomal protein 70 kDa
CCNB2AK0234040.0403808651.8138049Cyclin B2
CCDC121NM_0245840.0233710781.8025432Coiled-coil domain containing 121
ZNF563NM_1452760.018116261.7816929Zinc finger protein 563
PANK2AV7033940.0253171921.769196Pantothenate kinase 2
---N464360.0478411281.7669531---
ZFP28AW5904340.0114072251.7393188Zinc finger protein 28 homolog (mouse)
LOC284926BG8288170.041810461.7324702Hypothetical protein LOC284926
SLC24A1AF0261320.0017744471.7150456Solute carrier family 24 (sodium/potassium/calcium exchanger), member 1
---AU1469240.041542871.699999---
SOS2L206860.0192662331.6804754Son of sevenless homolog 2 (Drosophila)
UBE3BAL0967400.0483799651.6700492Ubiquitin protein ligase E3B
ELLAL5213910.038504271.6655054Elongation factor RNA polymerase II
SEZ6L2AF1317490.0085931951.6527929Seizure related 6 homolog (mouse)-like 2
MBNM_0053680.0240741241.650637Myoglobin
---BC0406280.0497947151.6501505---
MCOLN3NM_0182980.0304227231.6494503Mucolipin 3
---AK0215510.049946461.6114371---
---BF0621560.038067781.5880637---
FBXL17AW0022730.0033564241.5799221F-box and leucine-rich repeat protein 17
ZNF117BF1070060.0484313961.5662925Zinc finger protein 117
C1orf230AV7463310.0078921641.5605123Chromosome 1 open reading frame 230
---AA6500170.0494969561.5536357---
VKORC1L1NM_1735170.017242871.5391829Vitamin K epoxide reductase complex, subunit 1-like 1
MIR155HGBG2319610.0264137281.5365719MIR155 host gene (non-protein coding)
KCNAB1L398330.0246239081.534346Potassium voltage-gated channel, shaker-related subfamily, beta member 1
---AI8706340.0485820621.5243825---
YTHDC2AW9758180.0086610971.5151424YTH domain containing 2
CCNOBC0048770.0121149091.5041811Cyclin O
C5orf24AW0686150.0297834561.5023562Chromosome 5 open reading frame 24
---AV6484240.0323942561.5009412---
ADRBK2NM_0051600.0340591931.4894675Adrenergic, beta, receptor kinase 2
PIH1D2AI7447160.02454861.477943PIH1 domain containing 2
---BF2242180.0362180141.4755102---
---BF5915540.0420580361.474276---
GRIN2AN488960.0062765511.4638788Glutamate receptor, ionotropic, N-methyl D-aspartate 2A
RABL2A///RABL2BNM_0070820.009634151.4549305RAB, member of RAS oncogene family-like 2A///RAB, member of RAS oncogene family-like 2B
MYH14BC0006760.0093282511.4530606Myosin, heavy chain 14
LOC727820AW3405950.0186350181.4494766Hypothetical protein LOC727820
---AW0741430.046097721.448378---
ATP5G2X699090.0055486851.4429137ATP synthase, H+ transporting, mitochondrial F0 complex, subunit C2 (subunit 9)
MDM4AW2698130.0310213231.4353052Mdm4 p53 binding protein homolog (mouse)
C11orf84AI8665900.025362541.433334Chromosome 11 open reading frame 84
STYXAW9689350.0005155061.4238193 Serine/threonine/tyrosine interacting protein
S100A14NM_0206720.030425841.4226245S100 calcium binding protein A14
---BE5497800.0204345081.4224106---
NEURL4AL1368700.036546411.4173305Neuralized homolog 4 (Drosophila)
---AI8030100.0091079391.4132907---
ETV7AF2183650.0070535761.4130081Ets variant 7
RBBP9AL1218930.013811681.4109538Retinoblastoma binding protein 9
---AI2987550.0480689481.4096705---
LOC100130855AK0930770.0085857511.4052048Hypothetical protein LOC100130855
TSFMAI7968130.0058407061.4036938Ts translation elongation factor, mitochondrial

[i] DcR3, decoy receptor 3.

Hierarchical clustering analysis

The upregulated and downregulated genes were classified into 7 and 10 categories according to their biological functions, respectively (Fig. 1). The upregulated genes were associated with protein complex assembly, cell motility, regulation of transcription, cellular protein catabolic processes, cell membrane, nucleotide binding and glycosylation. The upregulated genes belonging to each cluster are listed in Table III. The downregulated genes were associated with transcription regulator activity, RNA biosynthetic processes, cytoskeleton, zinc finger region, protein complex assembly, phosphate metabolic processes, mitochondrion, ion transport, nucleotide binding and cell fractionation. The downregulated genes belonging to each cluster are listed in Table IV.

Table III

Functional categories of the 45 upregulated genes classified into 7 categories.

Table III

Functional categories of the 45 upregulated genes classified into 7 categories.

Functional categoryGenes
Protein complex assemblyCDH2, RANBP17, REPS2, TUBB2B, PEX13
Cell motilityCDH2, IL12B, PEX13
Regulation of transcriptionCDH2, ZC3H3, NUB1, DMRT2, ZBTB1, REPS2, SLC9A9, ZBTB10, THRB, CDH10, EGR3, ZNF681
Cellular protein catabolic processesZER1
Cell membraneCDH2, AGPAT9, RANBP17, SLC9A9, SLC16A6, C3AR1, CDH10, PEX13, DOK3
Nucleotide bindingRANBP17, TUBB2B,
GlycosylationCDH2, IL12B, SLC9A9, C3AR1, CDH10, C7orf58

Table IV

Functional categories of the 55 downregulated genes classified into 10 categories.

Table IV

Functional categories of the 55 downregulated genes classified into 10 categories.

Functional categoryGenes
Transcription regulator activityZNF563, ZFP28, ELL, ZNF117, CCNO, MDM4, ETV7, TSFM
RNA biosynthetic processesELL, ZNF117, ETV7, TSFM
CytoskeletonCep70, CCNB2, GRIN2A, MYH14
Zinc finger regionTPH1, ZNF563, ZFP28, SLC24A1, SOS2, ELL, MB, ZNF117, KCNAB1, GRIN2A, MDM4, S100A14, ETV7, RBBP9, TSFM
Protein complex assemblyMDM4
Phosphate metabolic processesADRBK2, ATP5G2, STYX
MitochondrionPANK2, ATP5G2, TSFM
Ion transportTREML4, SLC24A1, SEZ6L2, MB, MCOLN3, VKORC1L1, KCNAB1, GRIN2A, ATP5G2
Nucleotide bindingPANK2, YTHDC2, ADRBK2, RABL2A///RABL2B, MYH14
Cell fractionationCCNB2, SLC24A1, GRIN2A

Discussion

Among the 3 ligands of DcR3, TL1A (TNFSF15) is expressed by endothelial cells (12), macrophages (18,19), T cells (20,21), monocytes (22,23), dendritic cells (23), chondrocytes (24) and synovial fibroblasts (24), and contributes to the pathogenesis of cancer and autoimmune diseases via the apoptotic, stress, mitogenic and inflammation pathway by binding death receptor 3 (DR3) and DcR3 (12,25). The 3 ligands of DcR3 have been reported to contribute to the pathogenesis of RA (4,24,26,27). In these studies, DcR3 was considered a decoy receptor for ligands. We previously demonstrated that DcR3 binds to membrane-bound TL1A expressed on RA-FLS when it acts as a ligand in the pathogenesis of RA (16).

Genome-wide gene expression cDNA microarray is a powerful technique used to investigate the pathophysiology of a variety of diseases, including tumors (2830), immune-mediated diseases (31,32) and inflammatory diseases (3335). Using microarray, Chang et al revealed that genes characteristically expressed by tumor-associated macrophages were upregulated by DcR3 (30). In the current study, we first demonstrated the expression profiles of genes in RA-FLS regulated by DcR3.

We demonstrated that DcR3 regulates the expression of genes that are mainly associated with the upregulation of the protein complex assembly, cell motility and the regulation of transcription, and the downregulation of transcription regulator activity, RNA biosynthetic processes and cytoskeleton. We then focused on the following genes: cadherin 2, type 1, N-cadherin (neuronal) (CDH2), interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40) (IL12B), tryptophan hydroxylase 1 (TPH1), centrosomal protein 70 kDa (Cep70) and Zinc finger proteins as these genes were highly regulated, either upregulated or downregulated, and belonged to major functional clustering categories.

As for each gene, CDH2 has been reported to be associated with cell attachment and migration (36), metastatic potential (37), osteoblast differentiation (38) and the proliferation of RA-FLS (39).

IL12B encodes the IL-12B p40 subunit of IL-12 and IL-23 cytokines. IL-12 induces Th1 immune responses, and is thus linked with autoimmune diseases (40), while IL-23 is linked with autoimmune diseases via Th17 immune responses (41). IL-12 (42) and IL-23 (43,44) have also been reported to be involved in the pathogenesis of RA.

TPH1 is a rate-limiting enzyme involved in the synthesis of serotonin, and has been reported to be associated with the pathogenesis of RA through the inflammatory pathway (45) and bone biology (4648).

Cep70 was discovered in a proteomic study of the centrosome (49). Centrosomal activity is indispensable for the execution of cytokinesis and the progression of the cell cycle (50). Cep70 is crucial for mitotic spindle assembly (51) and promotes microtubule polymerization by increasing microtubule elongation (52).

Zinc finger proteins are involved in a broad range of biological activities, including double-stranded DNA binding, single-stranded DNA and RNA recognition, as well as coordinating protein-protein interactions (53).

In the current study, we first reported the expression profiles of genes in RA-FLS regulated by DcR3. Combined with our previous findings that DcR3 serves as a ligand by binding to membrane-bound TL1A on RA-FLS, our data demonstrate that DcR3 may regulate the gene expression of various key molecules in RA-FLS by binding to TL1A, thus affecting the pathogenesis of RA, such as proliferation, apoptosis, inflammation and bone biology. Further studies on the genes detected in the current study may provide a deeper understanding of the pathogenesis and treatment of RA by DcR3-TL1A signaling.

Acknowledgements

The authors thank Ms. Kyoko Tanaka, Ms. Minako Nagata, and Ms. Maya Yasuda for providing technical assistance. This study was supported by a Grant-in-Aid from the Health Science Research Grant of the Japanese Ministry of Education, Science and Culture (no. 24592261).

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October 2013
Volume 32 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Fukuda K, Miura Y, Maeda T, Takahashi M, Hayashi S and Kurosaka M: Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts. Int J Mol Med 32: 910-916, 2013
APA
Fukuda, K., Miura, Y., Maeda, T., Takahashi, M., Hayashi, S., & Kurosaka, M. (2013). Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts. International Journal of Molecular Medicine, 32, 910-916. https://doi.org/10.3892/ijmm.2013.1461
MLA
Fukuda, K., Miura, Y., Maeda, T., Takahashi, M., Hayashi, S., Kurosaka, M."Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts". International Journal of Molecular Medicine 32.4 (2013): 910-916.
Chicago
Fukuda, K., Miura, Y., Maeda, T., Takahashi, M., Hayashi, S., Kurosaka, M."Decoy receptor 3 regulates the expression of various genes in rheumatoid arthritis synovial fibroblasts". International Journal of Molecular Medicine 32, no. 4 (2013): 910-916. https://doi.org/10.3892/ijmm.2013.1461