Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide
Accumulating evidence from previous studies suggested that interleukin-1 (IL-1β) and tumor necrosis factor-α (TNF-α) play an important role in pathogenesis of temporomandibular disorders (TMD). However, the cell surface receptors and the intracellular signal pathways leading to these cytokines expre...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/329405 |
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| author | Xuefen Lin Jingjing Kong Qingting Wu Yingying Yang Ping Ji |
| author_facet | Xuefen Lin Jingjing Kong Qingting Wu Yingying Yang Ping Ji |
| author_sort | Xuefen Lin |
| collection | DOAJ |
| description | Accumulating evidence from previous studies suggested that interleukin-1 (IL-1β) and tumor necrosis factor-α (TNF-α) play an important role in pathogenesis of temporomandibular disorders (TMD). However, the cell surface receptors and the intracellular signal pathways leading to these cytokines expression are not fully understood. In the current study, we investigated the roles of Toll-like receptor 4 (TLR4) and its adaptor myeloid differentiation factor 88 (MyD88) in the expression of IL-1β and TNF-α in synovial fibroblasts (SFs) separated from rat temporomandibular joint (TMJ) with lipopolysaccharide (LPS) stimulation. The results showed that treatment with LPS could increase TLR4, MyD88, IL-1β, and TNF-α expression at both mRNA and protein levels. In addition, increased expression of IL-1β and TNF-α could be blocked by treatment with TAK-242, a blocker of TLR4 signaling, and also by MyD88 inhibitory peptide (MIP). These findings suggested that maybe TLR4/MyD88 signal transduction pathway participates in enhanced expression of IL-1 and TNF-α in patients with TMD. The activation of TLR4/MyD88 signal transduction pathway which results in production of proinflammatory factors may play a role in the pathogenesis of TMD. |
| format | Article |
| id | doaj-art-23de9bd3b41b44da8d3d7bcba12519f6 |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-23de9bd3b41b44da8d3d7bcba12519f62025-08-20T02:04:15ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/329405329405Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to LipopolysaccharideXuefen Lin0Jingjing Kong1Qingting Wu2Yingying Yang3Ping Ji4Stomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, ChinaStomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, ChinaStomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, ChinaStomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, ChinaStomatological Hospital of Shandong University, Number 44, Wen Hua Xi Lu, Shandong Province, Jinan 250012, ChinaAccumulating evidence from previous studies suggested that interleukin-1 (IL-1β) and tumor necrosis factor-α (TNF-α) play an important role in pathogenesis of temporomandibular disorders (TMD). However, the cell surface receptors and the intracellular signal pathways leading to these cytokines expression are not fully understood. In the current study, we investigated the roles of Toll-like receptor 4 (TLR4) and its adaptor myeloid differentiation factor 88 (MyD88) in the expression of IL-1β and TNF-α in synovial fibroblasts (SFs) separated from rat temporomandibular joint (TMJ) with lipopolysaccharide (LPS) stimulation. The results showed that treatment with LPS could increase TLR4, MyD88, IL-1β, and TNF-α expression at both mRNA and protein levels. In addition, increased expression of IL-1β and TNF-α could be blocked by treatment with TAK-242, a blocker of TLR4 signaling, and also by MyD88 inhibitory peptide (MIP). These findings suggested that maybe TLR4/MyD88 signal transduction pathway participates in enhanced expression of IL-1 and TNF-α in patients with TMD. The activation of TLR4/MyD88 signal transduction pathway which results in production of proinflammatory factors may play a role in the pathogenesis of TMD.http://dx.doi.org/10.1155/2015/329405 |
| spellingShingle | Xuefen Lin Jingjing Kong Qingting Wu Yingying Yang Ping Ji Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide Mediators of Inflammation |
| title | Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide |
| title_full | Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide |
| title_fullStr | Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide |
| title_full_unstemmed | Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide |
| title_short | Effect of TLR4/MyD88 Signaling Pathway on Expression of IL-1β and TNF-α in Synovial Fibroblasts from Temporomandibular Joint Exposed to Lipopolysaccharide |
| title_sort | effect of tlr4 myd88 signaling pathway on expression of il 1β and tnf α in synovial fibroblasts from temporomandibular joint exposed to lipopolysaccharide |
| url | http://dx.doi.org/10.1155/2015/329405 |
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