Ask about this productRelated genes to: MMP13 protein
- Gene:
- MMP13 NIH gene
- Name:
- matrix metallopeptidase 13
- Previous symbol:
- -
- Synonyms:
- CLG3
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-20
- Date modifiied:
- 2016-10-05
Related products to: MMP13 protein
Related articles to: MMP13 protein
- Osteoarthritis (OA) is a degenerative joint disease characterized by the failure of cartilage lubrication and persistent inflammation induced by friction-generated debris. Therefore, an effective OA treatment strategy should simultaneously enhance joint long-term lubrication and suppress inflammation. Toward this goal, we developed durable Lipo/PADM microgels via multiple cross-linking to integrate sustained lubrication with matrix metalloproteinase (MMP)-responsive dexamethasone release. The microgels maintained a low coefficient of friction of 0.029, remaining 24.3% lower than PBS after 8 weeks of in vitro degradation. In the MMP-rich OA microenvironment, ester-bond cleavage enabled sustained, on-demand drug release, reaching 70% within 14 days. Lipo/PADM microgels restored type II collagen expression, suppressed MMP-13 in bone marrow mesenchymal stem cells, and alleviated the OA-associated catabolic microenvironment. Intra-articular administration significantly reduced cartilage degeneration and delayed OA progression. These poly(glutamic acid)-based microgels offer a promising OA therapy through durable lubrication, responsive drug delivery, and prolonged intra-articular retention. - Source: PubMed
Wu RongChen YanyangWu JunyuRen KaixuanCui WenguoYin Jingbo - Rapid local drug clearance and poor sustained retention pose challenges to the treatment of osteoarthritis. Therefore, a local delivery system that prolongs intra-articular drug retention and achieves efficient targeted delivery holds significant clinical promise. - Source: PubMed
Publication date: 2026/09/09
Ban JunfengLi YichaoGuo YanhuaHe HuashenYang ChuangzanLi PeiningLiang JiaweiLi ShiruiLuo XueyuanLi YuXie YiLiu XiangmeiLi Xiaofang - Photobiomodulation (PBM) has shown potential for modulating osteoarthritis (OA)-related inflammation and cartilage degeneration, yet the irradiation conditions used across studies vary widely and are often assessed with selected marker-based endpoints. The transcriptomic responses associated withselected PBM condition PBM conditions in OA-like cells remain insufficiently defined. Here, we applied a controlled-variable screening design to identify an effective 660 nm PBM condition in IL-1β-induced OA-like SW1353 cells and further characterized the associated transcriptomic response. PBM was evaluated under different irradiances and energy densities using cell viability and IL6/MMP13 expression as representative inflammatory-catabolic readouts. Within the tested range, PBM generally reduced IL-1β-induced IL6 and MMP13 expression, and the inhibitory effect followed a biphasic-like, window-dependent pattern. Among the tested parameters, 5 mW/cm (18 J/cm total dose) produced the most consistent inhibitory effect. RNA sequencing (RNA-seq) under this selected condition revealed coordinated transcriptomic remodeling after PBM treatment. PBM suppressed major inflammatory-catabolic programs, including TNF, nuclear factor kappa B (NF-κB), IL-17, JAK-STAT, and cytokine-related signaling, while partially reversing IL-1β-associated alterations in cellular organization and metabolic pathways. PBM-reversed gene analysis identified 157 genes showing opposite expression trends between OA and PBM conditions. Protein-protein interaction (PPI) and IL6/MMP13-centered co-expression analyses indicated that PBM-responsive genes converged on cytokine/chemokine signaling, NF-κB-associated regulation, and extracellular matrix degradation modules. RT-qPCR validation confirmed the downregulation of representative nodes from these modules, including IRAK2, NFKBIA, TNFAIP3, IL6, CXCL8, CCL2, MMP13, and MMP3. These findings provide a transcriptomic framework for understanding PBM-associated regulation of inflammatory-catabolic responses in OA-like SW1353 cells. - Source: PubMed
Publication date: 2026/09/12
Miao XiaojingRen YiZhang XiaolinTian JingWu ChenghuiLiu TianyiZhang XuranLiu Muqing - Apoptosis and functional loss of articular chondrocytes serve as initiating events in temporomandibular joint osteoarthritis (TMJOA), and FoxO3 represents a critical molecule for sustaining chondrocyte homeostasis. This study investigates the regulatory mechanism of the lncRNA-OIP5-AS1/hsa-miRNA-223-3p/FoxO3 axis in TMJOA, aiming to identify potential therapeutic targets for this disease. Single-cell database analysis first revealed markedly reduced FoxO3 expression in TMJOA-derived chondrocytes. A rat TMJOA model was then constructed and assigned to control, model, and FoxO3 overexpression groups; micro-CT and histological staining, including HE and Safranin O-fast green staining, were applied to assess articular cartilage injury, while immunohistochemistry was used to detect cartilage-associated proteins Col2a1, MMP-13, Aggrecan, and ADAMTS-5. Further in vitro experiments validated the chondroprotective function of FoxO3 as well as the binding interaction between FoxO3 and rno-miRNA-223-3p. Database screening confirmed significant down-regulation of FoxO3 in TMJOA cartilage. Animal experiments demonstrated that FoxO3 overexpression mitigated chondrocyte injury in rat TMJOA lesions, increased Col2a1 and Aggrecan levels, and suppressed MMP-13 and ADAMTS-5 expression. Cellular assays showed that FoxO3 overexpression enhanced chondrocyte proliferation and matrix synthesis and preserved chondrocyte function. Sequencing and cellular evidence indicated that rno-miRNA-223-3p directly targets FoxO3 mRNA to repress its transcription and negatively modulate FoxO3 abundance, consequently aggravating chondrocyte apoptosis. Collectively, rno-miRNA-223-3p suppresses FoxO3 activity to facilitate TMJOA pathogenesis, and the lncRNA-OIP5-AS1/rno-miRNA-223-3p/FoxO3 regulatory cascade may act as a promising molecular target for TMJOA clinical intervention. - Source: PubMed
Xu XuesongQiao Shichong - Osteoarthritis (OA) is characterized by inflammatory and catabolic disruption of cartilage extracellular matrix (ECM) homeostasis. An increased relative abundance of activin receptor-like kinase 1 (ALK1) relative to ALK5, together with altered Smad signaling, has been associated with chondrocyte dysfunction during OA progression. This study examined whether eugenol attenuates IL-1β-induced ECM dysregulation in primary human chondrocytes and whether ALK1/ALK5-associated Smad signaling contributes to this response. Primary human chondrocytes were treated to IL-1β in the presence or absence of eugenol and analyzed using RT-qPCR, Western blotting, immunofluorescence, exploratory RNA sequencing, and siRNA-mediated loss-of-function experiments. Receptor-expression profiles were also assessed in juvenile and aged mouse cartilage and in cartilage from a previously established ACLT cohort. Eugenol attenuated IL-1β-induced decreases in ACAN, COL2A1, and SOX9 expression and reduced IL-1β-induced increases in MMP13, ADAMTS5, COL10A1, RUNX2, and IL-6 immunoreactivity. At the protein level, eugenol increased COL2A1 abundance and reduced MMP13 and ADAMTS5 level. Exploratory pairwise RNA-seq analysis identified IL-1β-responsive genes that were directionally counter-regulated by both eugenol concentrations; these genes were enriched in inflammatory, cell-behavior, and TGF-β/BMP-related pathways. Prolonged IL-1β exposure increased the ALK1/ALK5 protein ratio, primarily because ALK5 declined more markedly than ALK1. Eugenol treatment was associated with a lower ALK1/ALK5 ratio, reduced Smad1/5/9 phosphorylation, and increased Smad2/3 phosphorylation. ALK1 knockdown phenocopied selected eugenol-associated ECM responses, whereas ALK5 knockdown weakened several matrix-restorative and anti-catabolic responses. Computational docking, short molecular-dynamics simulations, and Y279A/H280A mutagenesis provided exploratory observations but did not demonstrate direct eugenol-ALK1 binding. In mouse cartilage, receptor-expression profiles differed between juvenile and aged animals, and eugenol partially normalized ACLT-associated changes in ALK1 and ALK5 immunostaining. These findings indicate that eugenol attenuates IL-1β-induced ECM dysregulation in chondrocytes. Modulation of ALK1/ALK5-associated Smad signaling may contribute to this response; however, direct target engagement and ligand-specific signaling mechanisms remain to be established. - Source: PubMed
Publication date: 2026/08/27
Wang YongcanWang YingLi ShanChen XiHou YaopuWang ChaoZhang YanzhuoTao JianfengWu ChengaiJiang Xu