Dataset Information

Hyperbaric oxygen protects type II collagen in interleukin-1?-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway.

ABSTRACT: The aim of this study was to explore the mechanisms of Hyperbaric oxygen (HBO) protective on interleukin-1? (IL-1?) induced rat's mandibular condylar chondrocytes. Chondrocytes were exposure to Hyperbaric oxygen after induced inflammatory by IL-1?. After that, the expression of p-JNK and c-Jun was increased significantly, while the Sox-9 was decreased significantly, Immunofluorescence results showed that the expression of p-JNK and p-c-Jun were decreased while the expression of Sox-9 and COL2 were increased in chondrocytes treated with IL-1? and selective JNK inhibitor. Hyperbaric oxygen might plays similar roles with the JNK-specific inhibitor SP600125, inducing the increase of Sox-9 and COL2 expression. On the whole, IL-1? induced inflammatory in chondrocytes by activating the JNK/c-Jun signaling pathway and down-regulate the expression of Sox-9 and COL2. However, Hyperbaric oxygen can inhibits IL-1? induced inflammatory response in chondrocytes though block the JNK/c-Jun signaling pathway and up-regulate the expression of Sox-9 and COL2.

SUBMITTER: Sun Q

PROVIDER: S-EPMC5601141 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Hyperbaric oxygen protects type II collagen in interleukin-1β-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway.

Sun Qi Q Wu Gaoyi G Chen Hang H Chen Lei L Chen Hongyu H Zhu Guoxiong G Zhao Huaqiang H

Oncotarget 20170717 36

The aim of this study was to explore the mechanisms of Hyperbaric oxygen (HBO) protective on interleukin-1β (IL-1β) induced rat's mandibular condylar chondrocytes. Chondrocytes were exposure to Hyperbaric oxygen after induced inflammatory by IL-1β. After that, the expression of p-JNK and c-Jun was increased significantly, while the Sox-9 was decreased significantly, Immunofluorescence results showed that the expression of p-JNK and p-c-Jun were decreased while the expression of Sox-9 and COL2 we ...[more]

PMID: 28947973

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Project description:Background: Functional orthoses are commonly used to treat skeletal Class II malocclusion, but the specific mechanism through which they do this has been a challenging topic in orthodontics. In the present study, we aimed to explore the effect of tensile stress on the osteogenic differentiation of condylar chondrocytes from an exosomal perspective. Methods: We cultured rat condylar chondrocytes under resting and tensile stress conditions and subsequently extracted cellular exosomes from them. We then screened miRNAs that were differentially expressed between the two exosome extracts by high-throughput sequencing and performed bioinformatics analysis and osteogenesis-related target gene prediction using the TargetScan and miRanda softwares. Exosomes cultured under resting and tensile stress conditions were co-cultured with condylar chondrocytes for 24 h to form the Control-Exo and Force-Exo exosome groups, respectively. Quantitative real time PCR(RT-qPCR) and western blotting were then used to determine the mRNA and protein expression levels of Runx2 and Sox9 in condylar chondrocytes. Results: The mRNA and protein expression levels of Runx2 and Sox9 in the Force-Exo group were significantly higher than those in the Control-Exo group (p < 0.05). The differential miRNA expression results were consistent with our sequencing results. Bioinformatics analysis and target gene prediction results showed that the main biological processes and molecular functions involved in differential miRNA expression in exosomes under tensile stress were biological processes and protein binding, respectively. Kyoto Gene and Genome Data Bank (KEGG) pathway enrichment analysis showed significant enrichment of differentially expressed miRNAs in the mTOR signaling pathway. The differentially expressed miRNAs were found to target osteogenesis-related genes. Conclusion: These results suggest that stimulation of rat condylar chondrocytes with tensile stress can alter the expression levels of certain miRNAs in their exosomes and promote their osteogenic differentiation. Exosomes under tensile stress culture conditions thus have potential applications in the treatment of Osteoarthritis (OA).

Project description:ObjectivesTo evaluate the cellular and matrix effects of botulinum toxin type A (Botox) on mandibular condylar cartilage (MCC) and subchondral bone.Materials and methodsBotox (0.3 unit) was injected into the right masseter of 5-week-old transgenic mice (Col10a1-RFPcherry) at day 1. Left side masseter was used as intra-animal control. The following bone labels were intraperitoneally injected: calcein at day 7, alizarin red at day 14 and calcein at day 21. In addition, EdU was injected 48 and 24 hours before sacrifice. Mice were sacrificed 30 days after Botox injection. Experimental and control side mandibles were dissected and examined by x-ray imaging and micro-CT. Subsequently, MCC along with the subchondral bone was sectioned and stained with tartrate resistant acid phosphatase (TRAP), EdU, TUNEL, alkaline phosphatase, toluidine blue and safranin O. In addition, we performed immunohistochemistry for pSMAD and VEGF.ResultsBone volume fraction, tissue density and trabecular thickness were significantly decreased on the right side of the subchondral bone and mineralized cartilage (Botox was injected) when compared to the left side. There was no significant difference in the mandibular length and condylar head length; however, the condylar width was significantly decreased after Botox injection. Our histology showed decreased numbers of Col10a1 expressing cells, decreased cell proliferation and increased cell apoptosis in the subchondral bone and mandibular condylar cartilage, decreased TRAP activity and mineralization of Botox injected side cartilage and subchondral bone. Furthermore, we observed reduced proteoglycan and glycosaminoglycan distribution and decreased expression of pSMAD 1/5/8 and VEGF in the MCC of the Botox injected side in comparison to control side.ConclusionInjection of Botox in masseter muscle leads to decreased mineralization and matrix deposition, reduced chondrocyte proliferation and differentiation and increased cell apoptosis in the MCC and subchondral bone.

Dataset Information

Hyperbaric oxygen protects type II collagen in interleukin-1?-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway.

Publications

Hyperbaric oxygen protects type II collagen in interleukin-1β-induced mandibular condylar chondrocyte via inhibiting the JNK/c-Jun signaling pathway.

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