Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritis chondrocytes

Liu, Yake; Zhu, Hai; Yan, Xin; Gu, Haoye; Gu, Zhifeng; Fan, Li

doi:10.1016/j.bbrc.2017.07.094

Cited by 42 publications

(50 citation statements)

References 47 publications

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“…With the consequence of chondrocytes apoptosis, articular homeostasis is compromised, which results in the destruction of cartilage and further accelerates pathological changes in OA, including gradually decreased chondrocytes, cartilage degeneration, and osteophyte formation [24]. Weakening the apoptotic process may ameliorate the development of cartilage degeneration.…”

Section: Discussionmentioning

confidence: 99%

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Zhou

Jiang

et al. 2018

Biochemical and Biophysical Research Communications

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Innate immune molecule surfactant protein D (SP-D), a member of the C-type lectin protein family, plays an indispensable role in host defense and the regulation of inflammation in the lung and other tissues. Osteoarthritis (OA) is a degenerative disease of cartilage, with inflammation that causes pathologic changes and tissue damage. However, it is unknown whether there exist SP-D expression and its potential role in the pathogenesis of OA. In this study, we examined SP-D expression and explored its biological function in a sodium nitroprusside (SNP)-stimulated rat chondrocytes and surgically-induced rat OA model. We found SP-D expression in both human and rat articular chondrocytes, with higher level in normal chondrocytes compared to in OA chondrocytes. Furthermore, In vivo study demonstrated that recombinant human SP-D (rhSP-D) ameliorated cartilage degeneration in surgically-induced rat OA model. In vitro cell culture study showed that rhSP-D markedly inhibited the expression of caspase-3 as an apoptosis biomarker, and decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK), which resulted in maintaining normal nuclear morphology and increasing mitochondrial membrane potential in SNP-stimulated rat chondrocytes. Collectively, these findings indicate that SP-D expresses in articular chondrocytes and suppresses SNP-stimulated chondrocyte apoptosis and ameliorates cartilage degeneration via suppressing p38 MAPK activity.

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Section: Discussionmentioning

confidence: 99%

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Zhou

Jiang

et al. 2018

Biochemical and Biophysical Research Communications

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“…Treatments that suppress chondrocyte apoptosis or enhance cell viability can achieve amelioration of OA, whereas increasing chondrocyte apoptosis or reducing cell viability may induce deterioration of OA. [ 2,8,31 ] Our study is in accordance with these previous conclusions. Tunicamycin (Tm), a glycosylation blocker, which may cause chondrocyte apoptosis and reduce cell viability, to establish an OA cell model.…”

Section: Discussionmentioning

confidence: 99%

“…[ 4,5 ] Endoplasmic reticulum stress (ERs) induced by endogenous and exogenous factors contributes to chondrocyte apoptosis in OA cartilage degeneration. [ 6‐8 ] Therefore, the symptoms of OA would be effectively alleviated by regulating ERs‐mediated apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Celastrol ameliorates endoplasmic stress-mediated apoptosis of osteoarthritis via regulating ATF-6/CHOP signalling pathway

Liu¹,

Zhang²,

Yang³

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives Osteoarthritis (OA) is a common degenerative joint disease with the pathological features of the reduced cartilage cellularity. Celastrol, a compound from Tripterygium wilfordii, exerted therapeutic effects on arthritis, but the potential mechanism remains unclear. Methods Tunicamycin was used to establish a model of OA in vitro, and ACLT surgery model in rats was applied to verify the mechanism. Chondrocytes were isolated from the knee articular cartilage of rabbit. MTT and flow cytometry assay were used to detect cell viability and apoptosis rate. Haematoxylin-eosin staining was used to assess for the histopathological changes. The activity and expression of apoptosis-related factors and ERs (endoplasmic reticulum stress)related factors were detected by ELISA, WB, PCR and IHC, respectively. Key findings Celastrol exhibited significant enhancement on cell viability and reduced the rate of apoptosis in Tm-exposed chondrocytes. Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. Celastrol showed a more significant effect on cell apoptosis rate and mRNA expression in the combination with 4-PBA.Conclusions This study reveals that celastrol may prevent OA by inhibiting the ERs-mediated apoptosis. All these might supply beneficial hints for celastrol on OA treatment.

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“…Then the suspension was strained with nylon cell strainer (100 µm) and washed with Dulbecco's modified Eagle's medium (DMEM) (Invitrogen; Thermo Fisher Scientific, Inc.). The isolated chondrocytes were cultured in DMEM supplemented with 10% fetal bovine serum (Gibco; Thermo Fisher Scientific, Inc.) at 37˚C with 5% CO 2 as reported (25).…”

Section: Methodsmentioning

confidence: 99%

LncRNA‑p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR‑451

et al. 2018

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Osteoarthritis (OA) is the most common type of arthritis, and remains to be social and medical challenge. Thus, identifying novel molecular targets is important for the prevention and treatment of OA. Long noncoding RNAs (lncRNAs) have been reported to modulate various biological and pathological processes. The aim of the present study was to investigate the role of lncRNA-p21 in OA and its underlying mechanism, in order to better understand the development of OA and its treatment. Chondrocytes were isolated from cartilage samples obtained from OA and normal patients. Chondrocytes were transfected with microRNA (miRNA/miR)-451 mimics, miR-451 inhibitor, pcDNA3.1(+)-p21 or small interfering RNA-p21. Flow cytometry was performed to analyze cell apoptosis and reverse transcription-quantitative polymerase chain reaction was conducted to detect the expression of mRNAs and miRNAs. Cell Counting Kit-8 assay was performed to detect cell viability. The results revealed that the level of lncRNA-p21 was significantly upregulated in OA cartilage when compared with the normal cartilage. Silencing of lncRNA-p21 increased cell viability and inhibited the apoptosis rate of chondrocytes in OA, while lncRNA-p21 overexpression decreased cell viability and increased the apoptosis rate of chondrocytes in OA. Overexpression of lncRNA-p21 suppressed the expression of miR-451 while the silencing of lncRNA-p21 reversed this effect. MiR-451 inhibitor effectively inhibited the upregulatory effect of si-p21 on miR-451. The increased cell viability and decreased apoptosis rate induced by lncRNA-p21 silencing was abolished by the miR-451 inhibitor. MiR-451 mimic effectively increased the downregulatory effect of pcDNA3.1-lncRNA-p21 on miR-451. The decreased cell viability and increased apoptosis rate induced by the overexpression of lncRNA-p21 was abolished by the miR-451 mimic. Investigation into the underlying mechanism revealed that lncRNA-p21 interacted with miRNA-451. In addition, lncRNA-p21 negatively regulated the expression of miR-451. Furthermore, lncRNA-p21 promoted the apoptosis of chondrocytes in OA by acting as a sponge for miR-451. Thus, lncRNA-p21 was proposed as a promising target for the treatment of OA.

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Endoplasmic reticulum stress participates in the progress of senescence and apoptosis of osteoarthritis chondrocytes

Cited by 42 publications

References 47 publications

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling

Celastrol ameliorates endoplasmic stress-mediated apoptosis of osteoarthritis via regulating ATF-6/CHOP signalling pathway

LncRNA‑p21 promotes chondrocyte apoptosis in osteoarthritis by acting as a sponge for miR‑451

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