Inhibition of HMGB1 suppresses inflammation and catabolism in temporomandibular joint osteoarthritis &lt;em&gt;via&lt;/em&gt; NF-κB signaling pathway

Li, Yan Yan; Feng, Y. T.; Liu, Li; Jin, Ke; Long, Xing

doi:10.4081/ejh.2022.3357

Cited by 5 publications

(6 citation statements)

References 44 publications

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“…Qiu and colleagues have reported an increased phosphorylated-NF-κB/NF-κB ratio in IL-1β-induced chondrocytes [77]. Li et al have described increased expression and nuclear localisation of p-NF-κB p65 in HMGB1-induced synovial fibroblasts from TMJOA [76]. Garcìa-Arnandis and colleagues showed that HMGB1-stimulated OA synoviocytes increased their transcriptional activity through NF-κB; however, the results did not reach statistical significance.…”

Section: Role Of Hmgb1 In Osteoarthritismentioning

confidence: 98%

“…HMGB1 has been shown to significantly increase MMP-13, ADAMTS-5, IL-1β, and IL-6 synthesis in human synovial fibroblasts from OA temporomandibular joint (TMJ) through NF-κB signalling [76]. It was shown that OA human chondrocytes, stimulated by recombinant dsHMGB1, increased synthesis of NF-κB1 (NF-κB p105 subunit) and NF-κB2 (NF-κB p100 subunit) mRNA, two NF-κB light chain enhancers [63].…”

Section: Role Of Hmgb1 In Osteoarthritismentioning

confidence: 99%

“…Additionally, late administration has not counteracted cartilage damage [68]. Last, Li and colleagues have demonstrated that intra-articular injections of anti-HMGB1 in TMJOA, induced by complete Freund's adjuvant administration in rats, ameliorate articular inflammation and cartilage destruction [76].…”

Section: Role Of S100b In Osteoarthritismentioning

confidence: 99%

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The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33

Palumbo,

Atzeni,

Murdaca

et al. 2023

IJMS

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Osteoarthritis (OA) is a multifactorial disease in which genetics, aging, obesity, and trauma are well-known risk factors. It is the most prevalent joint disease and the largest disability problem worldwide. Recent findings have described the role of damage-associated molecular patterns (DAMPs) in the course of the disease. In particular, alarmins such as HMGB1, IL-33, and S100B, appear implicated in enhancing articular inflammation and favouring a catabolic switch in OA chondrocytes. The aims of this review are to clarify the molecular signalling of these three molecules in OA pathogenesis, to identify their possible use as staging biomarkers, and, most importantly, to find out whether they could be possible therapeutic targets. Osteoarthritic cartilage expresses increased levels of all three alarmins. HMGB1, in particular, is the most studied alarmin with increased levels in cartilage, synovium, and synovial fluid of OA patients. High levels of HMGB1 in synovial fluid of OA joints are positively correlated with radiological and clinical severity. Counteracting HMGB1 strategies have revealed improving results in articular cells from OA patients and in OA animal models. Therefore, drugs against this alarmin, such as anti-HMGB1 antibodies, could be new treatment possibilities that can modify the disease course since available medications only alleviate symptoms.

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Section: Role Of Hmgb1 In Osteoarthritismentioning

confidence: 98%

Section: Role Of Hmgb1 In Osteoarthritismentioning

confidence: 99%

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The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33

Palumbo,

Atzeni,

Murdaca

et al. 2023

IJMS

View full text Add to dashboard Cite

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“…Osteoarthritis (OA) is a joint disease featuring degenerative articular cartilage and joint inflammation and is one of the main reasons for disability. 1 , 2 The accompanying pain and potential risks of physiological disability exert a great threat to public health worldwide. 3 Generally, the prevailing strategies for OA focus on pain management and symptom control.…”

Section: Introductionmentioning

confidence: 99%

Curculigoside inhibits osteoarthritis <em>via</em> the regulation of NLRP3 pathway

Wang,

Liu,

Zhou

et al. 2023

Eur J Histochem

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Osteoarthritis (OA) is characterized by degenerative articular cartilage. Nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) plays an important role in inflammation. This study aims to investigate whether protective effects of curculigoside on OA are medicated by the regulation of NLRP3 pathway. Destabilization of the medial meniscus (DMM) was performed to build an OA mouse model. After surgery, OA mice were treated with curculigoside. Immunohistochemistry was conducted to evaluate OA cartilage. In addition, human chondrocytes were isolated and treated with curculigoside. The mRNA and protein expression of iNOS, MMP-9, NLRP3 was detected by PCR and Western blot analysis. Curculigoside inhibited mRNA and protein levels of iNOS and MMP-9 induced by DMM surgery in a dose-dependent manner. Furthermore, the expression of NLRP3, NF-κB and PKR was downregulated after curculigoside administration. Moreover, curculigoside reversed the effects of IL-1β on MMP-9, iNOS and type II collagen expression at mRNA and protein levels in human chondrocytes in a dose-dependent manner. In conclusion, curculigoside exhibits beneficial effect on cartilage via the inhibition of NLRP3 pathway.

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“…High mobility group box-1 (HMGB1) is a member of a damage-associated molecular pattern (DAMP) protein. It stimulates the innate immune system and trigger inflammatory responses through binding to many cell surface receptors, including Toll-like receptors and receptors for advanced glycosylation end products (RAGE) [ 21 ]. HMGB1 has been demonstrated to be highly expressed in synovium and synovial fluid of patients with knee OA, and its levels in synovial fluid were related to the severity of synovitis and pain in patients [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0007292 promotes chondrocyte injury in osteoarthritis via targeting the miR-1179/HMGB1 axis

Lin

Tang

et al. 2023

J Orthop Surg Res

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Background Circular RNAs (circRNAs) have been demonstrated to participate in the progression of osteoarthritis (OA). This study aimed to investigate the role and molecular mechanism of hsa_circ_0007292 in OA. Methods Hsa_circ_0007292 was identified by analyzing a circRNA microarray from the Gene Expression Omnibus (GEO) database, and its expression was detected by real-time PCR in OA cartilage tissues and interleukin (IL)-1β-induced two human chondrocytes (CHON-001 and C28/I2), the OA cell models. The effects of hsa_circ_0007292 knockdown and miR-1179 overexpression on IL-1β-induced chondrocyte injury were examined by CCK-8, BrdU, flow cytometry, ELISA, and western blot. RNA pull-down assay and dual-luciferase reporter gene assay were used to analyze the interaction between hsa_circ_0007292 and miR-1179. Rescue experiments were carried out to determine the correlations among hsa_circ_0007292, miR-1179 and high mobility group box-1 (HMGB1). Results Hsa_circ_0007292 expression was upregulated in OA tissues and IL-1β-induced chondrocytes. Both downregulation of hsa_circ_0007292 and miR-1179 overexpression increased the proliferation and Aggrecan expression, suppressed apoptosis, matrix catabolic enzyme MMP13 expression and inflammatory factor (TNF‐α, IL‐6, and IL‐8) levels. There was a negative correlation between hsa_circ_0007292 and miR-1179, and a positive correlation between hsa_circ_0007292 and HMGB1 in OA tissues. The mechanistic study showed that hsa_circ_0007292 prevented HMGB1 downregulation by sponging miR-1179. Upregulation of HMGB1 could reverse the influence of hsa_circ_0007292 downregulation on IL-1β-induced chondrocyte injury. Conclusions Downregulation of hsa_circ_0007292 relieved apoptosis, extracellular matrix degradation and inflammatory response in OA via the miR-1179/HMGB1 axis, suggesting that hsa_circ_0007292 might be a potential therapeutic target for OA treatment.

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Inhibition of HMGB1 suppresses inflammation and catabolism in temporomandibular joint osteoarthritis <em>via</em> NF-κB signaling pathway

Cited by 5 publications

References 44 publications

The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33

The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33

Curculigoside inhibits osteoarthritis <em>via</em> the regulation of NLRP3 pathway

Hsa_circ_0007292 promotes chondrocyte injury in osteoarthritis via targeting the miR-1179/HMGB1 axis

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