Ask about this productRelated genes to: MMP13 antibody
- 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 antibody
Related articles to: MMP13 antibody
- Metaphyseal anadysplasia 1, which includes Spondyloepimetaphyseal dysplasia Missouri type, is a rare autosomal dominant skeletal dysplasia characterized by short stature, mild limb deformities, and transient metaphyseal irregularities that typically resolve with age. The condition is caused by heterozygous missense variants in the MMP13 gene, encoding matrix metalloproteinase 13, a key enzyme in endochondral ossification and extracellular matrix remodeling. Pathogenic variants in MMP13 are exceedingly rare, with only a few families reported. - Source: PubMed
Publication date: 2026/04/30
Thunström SofiaAntonsson PavelStenberg SimonAspholm Emelie ESwolin Eide Diana - Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage destruction, in which dysregulated chondrocyte apoptosis and impaired autophagy play critical roles, yet the upstream molecular drivers remain incompletely understood. Here, we identify pro-platelet basic protein (PPBP/CXCL7) as a previously unrecognized mediator of cartilage degeneration in OA. PPBP expression was markedly elevated in human OA cartilage, in the destabilization of the medial meniscus (DMM) mouse model, and in IL-1β-stimulated primary chondrocytes. Functional analyses revealed that PPBP overexpression augmented inflammatory and catabolic responses, suppressed autophagy, and promoted chondrocyte apoptosis, whereas PPBP knockdown preserved extracellular matrix homeostasis, enhanced LC3-associated autophagy, and reduced apoptotic cell death. Mechanistically, PPBP activation was associated with increased phosphorylation of PI3K and AKT and concomitant autophagy suppression; conversely, PPBP inhibition reduced PI3K and AKT phosphorylation, restored autophagic activity, and these protective effects were abolished by pharmacological autophagy inhibition using 3-methyladenine. Importantly, intra-articular silencing of PPBP in DMM mice attenuated cartilage erosion, preserved collagen II, reduced MMP13 expression, increased LC3 levels, and decreased chondrocyte apoptosis in vivo. Collectively, these findings establish PPBP as a key regulator of autophagy-apoptosis imbalance in OA chondrocytes and highlight PPBP as a potential therapeutic target for disease-modifying intervention in OA. - Source: PubMed
Publication date: 2026/04/30
Zhang HanHou KehaoMa XiaoSun GuantongKuai LeWang TianruiZhang YongtaoChen GuanhongHuang XiaohongZhang Yingze - Human breast milk (HBM) is an ideal nutritional source for the growth and development of infants. In addition, HBM contains hormones, growth factors, microRNAs and exosomes that perform various physiological functions. This study investigates the immunomodulatory effects of HBM-derived exosomes on myeloid cells and chondrocytes, and implications for juvenile idiopathic arthritis. HBM-derived exosomes were isolated and characterized using nanoparticle track analyzer and Western blotting. The HBM-derived exosomes treatment decreased the expression of inflammatory mediators and proinflammatory cytokines in mouse peritoneal macrophages upon lipopolysaccharide stimulation. Flow cytometry analysis of bone marrow-derived macrophages indicated that exosomes promoted M2 polarization, as evidenced by a decrease in cells expressing CD80 (M1 marker) and a concurrent increase in cells expressing M2 marker CD206. In addition, exosome treatment attenuated the mitogen-activated protein kinase signaling pathway by reducing the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase, and IκB-α, thereby reducing the expression of inducible nitric oxide synthase, cyclooxygenase-2, metalloprotease (MMP)-1, MMP-3, and MMP-13 in SW1353 chondrocytes following IL-1β stimulation. These findings suggest that HBM-derived exosomes promote macrophage polarization toward an anti-inflammatory M2 phenotype and exert significant immunomodulatory effects. - Source: PubMed
Publication date: 2026/04/30
Kwon DahyeonYoo Ji YoonDan Kang-BinKim Ki-UkLee Ji-YunMin Hyeyoung - Lipid nanoparticle (LNP) delivery of RNA therapeutics is constrained by poor tissue selectivity and off-target toxicity. Most high-throughput screening approaches have focused on single-target efficacy while overlooking off-target uptake. Here we report multiobjective LNP engineering with artificial intelligence (MOLEA), a system that integrates high-dimensional lipid representations, cell-type-resolved transfection data and multitask optimization to design ionizable lipids with both high potency and biological selectivity. MOLEA learns structure-function relationships across diverse cellular contexts to identify lipids that preferentially deliver mRNA to target tissue while minimizing hepatocyte transfection. Applying MOLEA to cartilage, we developed K9 LNPs, which achieve >90% transfection efficiency in mouse joint chondrocytes and a 13.5-fold increase in knee-to-liver selectivity compared to the clinical benchmark SM-102. We demonstrate chondrocyte-specific Mmp13 editing in osteoarthritis mouse models, leading to sustained cartilage protection and suppression of disease-associated immune and matrix remodeling. Our findings demonstrate how artificial-intelligence-guided multiobjective optimization can enable precision RNA delivery with potential applications to other tissues. - Source: PubMed
Publication date: 2026/04/28
Zhou MuyeXu YueLi GenChen JinganSavguira MargaritaSeto BreannaGong FanglinThomson TylerChen JuanLu Rick Xing ZeDong SongtaoChen DavidEileen ChristabelWu ShiqiZheng GangLi Bowen - Kruppel-like factor 15 (KLF15) is a transcription factor that promotes anabolic pathways and suppresses catabolic signalling in joint tissues. KLF15 regulates adipocyte differentiation through peroxisome proliferator-activated receptor-γ (PPARγ), which suppresses inflammation via the nuclear factor-κB pathway. This study aimed to clarify the effects of KLF15 in a mouse model of collagen antibody-induced arthritis (CAIA). - Source: PubMed
Publication date: 2026/04/28
Anjiki KHayashi SKikuchi KTakashima YIkuta KWada KTachibana SOnoi YSuda YSaito AMaeda TKamenaga TTsubosaka MKuroda YNakano NMatsumoto THosooka TOgawa WKuroda R