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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:Background Extracellular matrix (ECM) protein malfunction or defect may lead to temporomandibular joint osteoarthritis (TMJ OA). Dentin sialophophoprotein (DSPP) is a mandibular condylar cartilage ECM protein, and its deletion impacted cell proliferation and other extracellular matrix alterations of postnatal condylar cartilage. However, it remains unclear if long-term loss of function of DSPP leads to TMJ OA. The study aimed to test the hypothesis that long-term haploinsufficiency of DSPP causes TMJ OA. Materials and Methods To determine whether Dspp+/- mice exhibit TMJ OA but no severe tooth defects, mandibles of wild-type (WT), Dspp+/-, and Dspp homozygous (Dspp-/-) mice were analyzed by Micro-computed tomography (micro-CT). To characterize the progression and possible mechanisms of osteoarthritic degeneration over time in Dspp+/- mice over time, condyles of Dspp+/- and WT mice were analyzed radiologically, histologically, and immunohistochemically. Results Micro-CT and histomorphometric analyses revealed that Dspp+/- and Dspp-/- mice had significantly lower subchondral bone mass, bone volume fraction, bone mineral density, and trabecular thickness compared to WT mice at 12 months. Interestingly, in contrast to Dspp-/- mice which exhibited tooth loss, Dspp+/- mice had minor tooth defects. RNA sequencing data showed that haplodeficency of DSPP affects the biological process of ossification and osteoclast differentiation. Additionally, histological analysis showed that Dspp+/- mice had condylar cartilage fissures, reduced cartilage thickness, decreased articular cell numbers and severe subchondral bone cavities, and with signs that were exaggerated with age. Radiographic data showed an increase in subchondral osteoporosis up to 18 months and osteophyte formation at 21 months. Moreover, Dspp+/- mice showed increased distribution of osteoclast in the subchondal bone and increased expression of MMP2, IL-6, FN-1, and TLR4 in the mandibular condylar cartilage. Conclusions Dspp+/- mice exhibit TMJ OA in a time-dependent manner, with lesions in the mandibular condyle attributed to hypomineralization of subchondral bone and breakdown of the mandibular condylar cartilage, accompanied by upregulation of inflammatory markers.

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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