Ask about this productRelated genes to: MMP3 antibody
- Gene:
- MMP3 NIH gene
- Name:
- matrix metallopeptidase 3
- Previous symbol:
- STMY1, STMY
- Synonyms:
- -
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: MMP3 antibody
Related articles to: MMP3 antibody
- Current therapies for osteoarthritis (OA) focus on symptom management, rather than halting disease progression. Vasoactive intestinal peptide (VIP) has shown promising effects in musculoskeletal diseases, preserving joint integrity and modulating inflammation. This study investigates the potential of VIP to promote chondrogenic differentiation of human bone marrow mesenchymal stem cells (BM-hMSC) and to modulate inflammatory and cartilage extracellular matrix (ECM)-degrading mediators in human osteoarthritis articular chondrocytes (OA-hAC). BM-hMSC from healthy donors were cultured in 3D pellet sytems under chondrogenic conditions, with or without VIP, for up to 21 days. Chondrogenesis was evaluated through the expression of key markers (SOX9, COL2A1, and ACAN), hypertrophic markers (RUNX2, COL10A1, and MMP13), and glycosaminoglycans (GAG). VIP accelerated chondrogenic differentiation by inducing earlier mRNA and protein expression of chondrogenic markers and enhancing GAG production. In parallel, OA-hAC were cultured in 3D alginate microbeads and stimulated with fibronectin fragments (Fn-fs) in the presence and absence of VIP. We analysed the effects of VIP on cell proliferation, GAG production, and the modulation of complement components (C1R and C3) and matrix metalloproteinases (MMP1, MMP3, MMP9, and MMP13). VIP increased cell proliferation and GAG deposition while significantly reducing the production of complement component C1R and matrix metalloproteinases MMP1 and MMP13. Overall, these findings demonstrate that VIP advances chondrogenesis and exerts anti-inflammatory and anti-catabolic effects in 3D culture models. This study highlights the potential of VIP as a therapeutic agent and supports the combination of MSC-based approaches with VIP as a promising strategy to enhance cartilage regeneration and slow OA progression. - Source: PubMed
Publication date: 2026/05/25
Tecza KarolinaRodríguez-Hernández CristinaVillanueva-Romero RaúlCastro-Vázquez DavidCabrera-Martín AliciaArribas-Castaño PaulaCarrión MarGutiérrez-Cañas IreneLargo RaquelCalamia ValentinaBlanco Francisco JGomariz Rosa PJuarranz YasminaMartínez CarmenPérez-García Selene - Intervertebral disc degeneration (IVDD) is the primary cause of spinal degenerative diseases. Nucleus pulposus (NP) cell senescence is a significant pathological manifestation of IVDD. Here, we constructed a hypoxia-induced NP cell model to clarify the mechanisms by which S-palmitoylation is involved in NPC senescence. The IP3R S-palmitoylation of NP cells was significantly reduced under hypoxic conditions, contributing to abnormalities in mitochondria-associated membranes (MAMs). The study found that cellular expression of Bax, Bcl-2, Cleaved-Caspase8, Cleaved-Caspase3, MMP3, and MMP13 was promoted, while COL2 and AGG expression was inhibited. The up-regulated palmitoylation-modifying enzyme DHHC6 can promote IP3R S-palmitoylation modification and regulate GRP75, VDAC1, Drp1, and Mfn2 expression. It can inhibit apoptosis in NP cells, reduce intracellular calcium and ROS levels, elevate mitochondrial membrane potential, and reduce γ-H2AX expression levels. It also inhibited the protein expression levels of hypoxia-induced apoptosis molecules, matrix-degrading enzymes, and up-regulated extracellular matrix protein expression. These results suggested that hypoxia-induced IP3R depalmitoylation might play a role in structural and functional abnormalities in MAMs, which trigger senescence in NP cells. - Source: PubMed
Publication date: 2026/05/22
Liang QiZhang JianfengYan JingchuanGuo WeidongZhao JianLin LiLi ShuangFeng DaxiongLiao Bo - Traditional Chinese medicine QingYiHuaJi formula (QYHJ) has anti-tumor effect in Pancreatic adenocarcinoma (PAAD). However, the potential mechanism and key targets of QYHJ have not been fully elucidated. - Source: PubMed
Han JintaoQian FuchuShi Jiemin - Osteoarthritis (OA), characterized by oxidative stress and inflammatory damage, poses significant challenges in achieving effective local drug concentrations and sustaining reactive oxygen species (ROS) clearance. This study developed a nanoparticle, FeO@ZIF-8, endowed with superoxide dismutase (SOD)- and catalase (CAT)-like enzyme-mimetic activities. The nanocomposite not only synergistically neutralizes key ROS but also significantly alleviates oxidative stress and inflammatory responses in chondrocytes by modulating SIRT1/Nrf2 axis. More importantly, the introduction of an external magnetic field (MF) was demonstrated to markedly enhance cellular uptake and retention of the nanoparticles, thereby providing superior cartilage protection and tissue repair compared to non-targeted intervention. Macroscopic and histological evaluations confirmed that the cartilage morphology and matrix composition in the FeO@ZIF-8 + MF group closely resembled those of healthy tissue, accompanied by notable downregulation of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and catabolic enzymes (MMP-3, MMP-13). These findings highlight the potential of magnetically guided nanozyme therapy as a novel and efficacious approach for OA treatment, offering a multimodal solution to modulate the disease microenvironment and enhance regenerative outcomes. - Source: PubMed
Publication date: 2026/05/22
Li ZongruLi BingxianWang ZheweiSathasivami ThenapakiamLi XiudongZheng LiKai DanLan YingZhao Jinmin - Matrix metalloproteinase (MMP) gene polymorphisms have been implicated in cancer susceptibility; however, the results from previous studies have been inconsistent across populations and tumor types. The present study aimed to systematically evaluate the associations between MMP-1, MMP-3 and MMP-8 polymorphisms and cancer risk through a comprehensive meta-analysis. A total of 36,368 cancer cases and 40,246 controls from eligible studies were included. Pooled odds ratios and 95% confidence intervals were calculated to assess the associations between selected MMP polymorphisms and cancer risk. Venice criteria and false-positive report probability were applied to evaluate the cumulative evidence. Subgroup analyses according to ethnicity, genetic model and cancer type were conducted. Functional annotation was also integrated to explore potential biological mechanisms. In total, three polymorphisms (MMP-3 rs35068180, MMP-3 rs3025058 and MMP-1 rs1799750) were found to be significantly associated with the risk of seven types of cancer. Of these, strong evidence was assigned to two single nucleotide polymorphisms for three cancer risks (four associations), including MMP-3 rs3025058 with esophageal cancer in all populations under the dominant model, MMP-1 rs1799750 with glioblastoma in all populations under the recessive model and MMP-1 rs1799750 with renal cancer in all populations under both the recessive and allelic models. A total of six associations showed moderate evidence, while 14 were classified as weak. Notably, the effect sizes and statistical significance varied by ethnicity, genetic model and cancer type, suggesting context-dependent and population-specific effects. Functional annotation indicated that key variants may affect gene expression and tumor biology via regulation of promoter or enhancer activity. No significant association was observed between MMP-8 polymorphisms and cancer risk. The findings provide new insights into the complexity of gene-environment interactions underlying cancer susceptibility. This comprehensive meta-analysis highlights the complex, context-dependent associations of MMP-1, MMP-3 and MMP-8 polymorphisms with cancer risk. The results of the present study underscore the need for large, multi-ethnic studies and integrated genomic, functional and environmental analyses to clarify the roles of MMP variants in cancer development and to identify high-risk populations for precision prevention. - Source: PubMed
Publication date: 2026/05/07
Xu SuqinLiu XianpingHuang Chenglu