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Knockdown of long non?coding RNA AK094629 attenuates the interleukin?1? induced expression of interleukin?6 in synovium?derived mesenchymal stem cells from the temporomandibular joint.

ABSTRACT: Interleukin (IL)?1? is a key promotor in the pathogenesis of temporomandibular joint osteoarthritis. Differentiation of stem cells to cartilage is a crucial repair mechanism of articular cartilage damage, and IL?1? has been reported to impede the differentiation by upregulating the secretion of IL?6, an important inflammatory factor. Long non?coding RNAs (lncRNAs) regulate a number of physiological and pathological processes, but whether lncRNA AK094629 contributes to the IL?1? mediated induction of inflammation remains unclear. Therefore, the aim of the present study was to investigate the effect of AK094629 on IL?1??induced IL?6 expression in synovial?derived mesenchymal stem cells (SMSCs) of the temporomandibular joints. The results of the present study demonstrated that the expression of AK094629 in the synovial tissue of patients with osteoarthritis was positively correlated with IL?1?. In addition, IL?1? upregulated the expression of AK094629 in the SMSCs in vitro, and AK094629 knockdown inhibited the IL?1? mediated upregulation of IL?6. The present study also demonstrated that AK094629 knockdown downregulated the expression of the mitogen?activated protein kinase kinase kinase 4 (MAP3K4), which is upregulated by IL?1?, whereas knockdown of MAP3K4 did not affect the expression of AK094629, but reversed the upregulation of IL?6 in SMSCs. In conclusion, AK094629 knockdown attenuated the expression of IL?1??regulated IL?6 in the SMSCs of the temporomandibular joint by inhibiting MAP3K4. Therefore, AK094629 may be a potential novel therapeutic target for the treatment of temporomandibular joint osteoarthritis.

SUBMITTER: Jia J

PROVIDER: S-EPMC7339665 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Knockdown of long non‑coding RNA AK094629 attenuates the interleukin‑1β induced expression of interleukin‑6 in synovium‑derived mesenchymal stem cells from the temporomandibular joint.

Jia Jiaxin J Sun Jiadong J Liao Wenting W Qin Lingling L Su Kai K He Yiqing Y Zhang Jiaqiang J Yang Ronchung R Zhang Zhiguang Z Sun Yangpeng Y

Molecular medicine reports 20200528 2

Interleukin (IL)‑1β is a key promotor in the pathogenesis of temporomandibular joint osteoarthritis. Differentiation of stem cells to cartilage is a crucial repair mechanism of articular cartilage damage, and IL‑1β has been reported to impede the differentiation by upregulating the secretion of IL‑6, an important inflammatory factor. Long non‑coding RNAs (lncRNAs) regulate a number of physiological and pathological processes, but whether lncRNA AK094629 contributes to the IL‑1β mediated inductio ...[more]

PMID: 32468015

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Project description:BackgroundsAbnormal cartilage calcification is one of the pathological changes of temporomandibular joint (TMJ) osteoarthritis (OA). Recent studies have reported that exosomes can regulate the formation of abnormal calcified nodules in diseases including atherosclerosis and chronic kidney disease. However, the influences of chondrocyte-derived exosomes on abnormal cartilage calcification in TMJ OA are still unclear.MethodsTMJ OA was induced by unilateral anterior crossbite (UAC) for 4, 8, or 12 weeks in rats to observe abnormal calcification in TMJ condylar cartilage and exosome formation. Concomitantly, GW4869, the inhibitor of exosome formation, was locally injected to the TMJ of rats under stimulation of UAC, while the exosomes extracted from primary condylar chondrocytes stimulated with fluid flow shear stress (FFSS) were locally injected to rats TMJ.ResultsAbnormal calcification was enhanced in the degenerative cartilage of TMJ OA in UAC rats, and a large number of exosome-like structures with diameters of 50-150 nm were found in the calcified cartilage together with decreased expression of matrix Gla protein (MGP) and increased expression of CD63, tissue-nonspecific alkaline phosphatase (TNAP) and nucleotide pyrophosphatase/phosphodiesterase-1 (NPP1). After FFSS stimulation, the number of exosomes secreted by chondrocytes and the numbers of calcified nodules were increased in cultured cells, and the protein levels of MGP, TNAP, and NPP1 in exosomes were changed. Inhibition of exosome formation, TNAP, and NPP1 or supplementation with exogenous MGP effectively alleviated FFSS-induced chondrocyte calcification. Local injection of GW4869, the exosome inhibitor, alleviated TMJ OA-related cartilage degeneration and calcification in UAC rats. Local injection of exosomes obtained from chondrocytes stimulated by FFSS to the TMJs of normal rats induced cartilage degeneration and calcification similar to that in TMJ OA.ConclusionsAbnormal biomechanical loading leads to enhanced formation of chondrocyte-derived exosomes, in which promoters of calcification increased and inhibitors decreased, resulting in accelerating abnormal cartilage calcification in TMJ OA. The inhibition of degenerative chondrocyte-derived exosomes is expected to be a new way to prevent and treat TMJ OA.

Dataset Information

Knockdown of long non?coding RNA AK094629 attenuates the interleukin?1? induced expression of interleukin?6 in synovium?derived mesenchymal stem cells from the temporomandibular joint.

Publications

Knockdown of long non‑coding RNA AK094629 attenuates the interleukin‑1β induced expression of interleukin‑6 in synovium‑derived mesenchymal stem cells from the temporomandibular joint.

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