Establishing SW1353 Chondrocytes as a Cellular Model of Chondrolysis

Pang, Kok-Lun; Chow, Yoke Yue; Leong, Lek Mun; Law, Jia Xian; Ghafar, Norzana Abd; Soelaiman, Ima Nirwana; Chin, Kok‐Yong

doi:10.3390/life11040272

Cited by 17 publications

(16 citation statements)

References 90 publications

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“…Among the cytokines related to inflammation, IL-1β promotes the generation and release of several inflammatory mediators, including TNF-α, inducible nitric oxide synthase (iNOS), and MMPs, all of which contribute to chondrocyte dysfunction and ECM degradation [ 26 – 28 ]. For this reason, IL-1β is widely applied to establish models of cellular OA [ 29 , 30 ]. Treatment with IL-1β in SW1353 cells is not an ideal cell model, but it is a good tool for investigating inflammation.…”

Section: Discussionmentioning

confidence: 99%

Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway

et al. 2022

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Objectives This study aims to investigate the effects of Icariin (ICA) on interleukin-1β (IL-1β)-induced osteoarthritis (OA) and its potential mechanism of action. Methods SW1353 chondrocytes were pretreated with ICA for 2 h, followed by stimulation with IL-1β to mimic OA. Expression levels of matrix metalloproteinases (MMP-3) and collagen II were determined using real-time PCR and Western blot assays. Autophagy activation (by ICA) or inhibition (by shRNA) was determined based on the expression levels of ULK1, Beclin-1, LC3-II/I, and p62, using Western blot analysis. The phosphorylation levels of PI3K, Akt, mTOR, and ULK1 were also detected using Western blot analysis. Results IL-1β increased MMP-3 overproduction, induced collagen II degradation, and reduced the level of autophagy-associated proteins, including ULK1, Beclin-1, and LC3-II/I. In contrast, ICA pretreatment attenuated IL-1β-induced MMP-3 overproduction, increased collagen II expression, and induced expression of autophagy-related proteins. ICA also decreased PI3K, Akt, and mTOR phosphorylation, increased the production of ULK1, and induced autophagy. Short hairpin RNA-mediated knockdown of ULK1 led to activation of the PI3K/Akt/mTOR pathway, which reversed the protective effects of ICA. Conclusions Our findings indicate that ICA can induce autophagy by regulating the PI3K/AKT/mTOR/ULK1 signaling pathway. This study suggests that ICA may be effective for treating OA.

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Section: Discussionmentioning

confidence: 99%

Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway

et al. 2022

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“…Indeed, these cell lines were already used as an in vitro cellular model resembling osteoarthritis and rheumatoid arthritis, respectively. 57 , 58 We verified that both SW1353 and SW982 internalized EVs isolated from untreated HaCaT cells, even if with different kinetics ( Figure 5 ). SW1353 cells internalize EVs in a superimposable way to HaCaT acceptor cells (compare Figure 5A with Supplementary Figure 1B ) whereas SW982 cells display a reduced internalization rate.…”

Section: Discussionmentioning

confidence: 53%

Potential Pathogenetic Role of Antimicrobial Peptides Carried by Extracellular Vesicles in an in vitro Psoriatic Model

Capriotti¹,

Iuliano²,

Lande³

et al. 2022

JIR

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Purpose Extracellular Vesicles (EVs) are a heterogeneous group of cell-derived membranous nanoparticles involved in several physiopathological processes. EVs play a crucial role in the definition of the extracellular microenvironment through the transfer of their cargo. Psoriasis is a prototypical chronic inflammatory disease characterized by several secreted mediators, among which antimicrobial peptides (AMPs) are considered pivotal in the development of the psoriatic inflammatory microenvironment. The role of EVs in the pathogenesis of psoriasis has not been elucidated yet, even if emerging evidence demonstrated that interleukin-17A (IL-17A), the psoriasis-related principal cytokine, modifies EVs release and cargo content. The aim of this work was to analyze whether, besides IL-17A, other psoriasis-related cytokines (ie, IFN-γ, TNF-α, IL-22 and IL-23) could affect EVs release and their AMPs mRNAs cargo as well as to analyze the potential biological effect due to EVs internalization by different acceptor cells. Methods Nanoparticle tracking analysis (NTA) was performed on supernatants of HaCaT cells stimulated with IL-17A, IFN-γ, TNF-α, IL-22 or IL-23 to enumerate EVs. Real-Time RT-PCR was used for gene expression analysis in cells and EVs. Confocal microscopy and Flow cytometry were used to, respectively, study Netosis and EVs internalization. Results IL-17A and IFN-γ increased EVs release by HaCaT cells. All the tested cytokines modulated AMPs mRNA expression in parental cells and in their respective EVs. S100A12 and hBD2 mRNAs were upregulated following IL-17A and IL-22 treatments. Interestingly, EVs derived from cytokine treated HaCaT cells induced Netosis in freshly isolated neutrophils. Upregulation of S100A12 and hBD2 mRNA was also detectable in acceptor cells incubated with EVs derived from cells treated with psoriasis-related cytokines. Conclusion The obtained results highlighted the role of EVs in the composition of psoriasis-associated secretome and microenvironment also suggesting the EV involvement in the spreading of the disease mediators and in the possible associated comorbidities.

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“…Treating chondrocytes with MIA has been shown to cause mitochondrial dysfunction and, subsequently, cell death [26,27]. In another study, MIA arrested chondrocyte proliferation due to S-phase arrest [28]. MIA has been commonly used to induce cartilage damage in animals to mimic osteoarthritis in humans [29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Effects of Palm Tocotrienol-Rich Fraction Alone or in Combination with Glucosamine Sulphate on Grip Strength, Cartilage Structure and Joint Remodelling Markers in a Rat Model of Osteoarthritis

et al. 2021

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Background: Osteoarthritis is a degenerative joint disease lacking disease-modifying therapeutic agents. This study aimed to compare the effects of palm tocotrienol-rich fraction (TRF), glucosamine sulphate, and both agents combined in rats with osteoarthritis induced by monosodium iodoacetate (MIA). Methods: Thirty adult male rats were randomized into normal control, and osteoarthritis groups were treated orally daily with vehicle, palm TRF (100 mg/kg), glucosamine sulphate (250 mg/kg), and both agents combined for 4 weeks. Body weight and grip strength were measured weekly. After being sacrificed, the joints and blood were harvested for histology and serum cartilage oligomeric matrix protein (COMP) levels. Results: The body weight of the rats receiving treatment rebounded significantly after an initial reduction (vs osteoarthritic control, p < 0.05). The rats receiving combined treatments showed significantly better grip strength than the osteoarthritic control and individual treatment groups (p < 0.05). The serum COMP level was lower in all the treated groups (vs osteoarthritic control, p < 0.05). Cartilage histology of the treated rats was not significantly improved (vs osteoarthritic control, p > 0.05). Conclusion: The combination of palm TRF and glucosamine sulphate was more effective than individual agents in improving the grip strength of the rats, but the cartilage damage might need more time to heal.

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Establishing SW1353 Chondrocytes as a Cellular Model of Chondrolysis

Cited by 17 publications

References 90 publications

Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway

Icariin alleviates osteoarthritis through PI3K/Akt/mTOR/ULK1 signaling pathway

Potential Pathogenetic Role of Antimicrobial Peptides Carried by Extracellular Vesicles in an in vitro Psoriatic Model

Effects of Palm Tocotrienol-Rich Fraction Alone or in Combination with Glucosamine Sulphate on Grip Strength, Cartilage Structure and Joint Remodelling Markers in a Rat Model of Osteoarthritis

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