MMP12
- Known as:
- MMP12
- Catalog number:
- Y214461
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MMP12
Related genes to: MMP12
- Gene:
- MMP12 NIH gene
- Name:
- matrix metallopeptidase 12
- Previous symbol:
- -
- Synonyms:
- HME
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-18
- Date modifiied:
- 2015-02-23
Related products to: MMP12
Related articles to: MMP12
- Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of interstitial lung disease (ILD). However, the causal role of MMPs in ILD pathogenesis remains to be elucidated. This study aimed to investigate the causal effects of circulating MMPs on ILD risk and to evaluate whether immune cell phenotypes mediate this relationship. A comprehensive Mendelian randomization (MR) and mediation analysis was conducted using publicly available data of genome-wide association study (GWAS) summary statistics. Genetic instruments for 6 MMPs (MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, and MMP-12) and 731 immune cell traits were selected. Inverse-variance weighted (IVW) was the primary analytical method, supplemented by other MR techniques. Sensitivity analyses included MR-Egger regression, Cochran Q test, and MR-PRESSO to assess pleiotropy and heterogeneity. Mediation analysis was performed to quantify the proportion of the effect mediated by significant immune cells. Genetically predicted MMP-9 levels showed a significant positive causal effect on ILD risk (odds ratio [OR] = 1.034, 95% confidence interval [CI]: 1.006-1.064, P = .018). Among 731 immune cell phenotypes, 8 were identified as causal for ILD, including effector memory double negative T cells (EM DNT; OR = 1.170, P = .001). MMP-9 was further found to increase the abundance of EM DNT (OR = 1.041, 95% CI: 1.009-1.074, P = .012). Mediation analysis indicated that EM DNT mediated 18.5% of the total effect of MMP-9 on ILD. Sensitivity analyses revealed no evidence of horizontal pleiotropy or significant heterogeneity. This study provides genetic evidence supporting a causal role of MMP-9 in the development of ILD, partially mediated through EM DNT. These findings suggest that MMP-9 and EM DNT could be potential therapeutic targets for preventing or treating ILD. - Source: PubMed
Ren QijieSun FengyuanYang LeileiSu DingleiShen Minning - Non-small cell lung cancer (NSCLC) remains a major cause of cancer mortality. The Tumor Immune Dysfunction and Exclusion (TIDE) score is widely used to estimate immune-checkpoint blockade response, but its broader prognostic relevance in unselected NSCLC populations is unclear. This study aimed to determine whether TIDE-informed strata carry prognostic information beyond immunotherapy settings, and to develop and externally validate an immune gene expression-based prognostic signature derived from differentially expressed genes (DEGs) between these strata. - Source: PubMed
Publication date: 2026/02/26
Zhou JiaxuanLi NaLi ZimengChen JinmiaoDu YifeiLi XinchunWan Qi - Myocardial infarction (MI) triggers massive cardiomyocyte loss, inflammatory and fibrotic remodeling, and disruption of electrical conduction, which are difficult to reverse with a single therapeutic modality. Pathologically, the infarcted myocardium undergoes a sequential transition from local acidosis to oxidative/inflammatory injury and finally matrix metalloproteinase-driven scar formation. Guided by these stage-specific cues and the need to restore electrical continuity, we designed an injectable conductive hydrogel (PGO/CAM@Sal) that integrates a polypyrrole-based conductive network with pH/reactive oxygen species (ROS)/matrix metalloproteinase-9 (MMP9) triple-responsive salidroside delivery. The hydrogel matches myocardial stiffness, exhibits favorable injectability, self-healing and tissue adhesion, shows electrical conductivity comparable to native myocardium, and enables on-demand salidroside release under MI-mimicking conditions. In vitro, PGO/CAM@Sal effectively scavenges ROS, suppresses pro-inflammatory cytokine production, promotes M2 macrophage polarization and angiogenesis, and enhances connexin-43 expression and cardiomyocyte electrical coupling. In a rat MI model, local injection of PGO/CAM@Sal bridges the non-conductive infarct, stabilizes ventricular electrophysiology, improves conduction velocity and homogeneity, reduces arrhythmia vulnerability, and concurrently attenuates fibrosis, hypertrophy, and adverse left ventricular remodeling, leading to marked recovery of systolic function. Transcriptomic analysis suggests a potential involvement of the Mmp12/Cybb axis and related pathways involved in inflammation, oxidative stress, fibrosis, calcium handling, and ion transport. These molecular alterations were further validated by qRT-PCR and immunohistochemical analyses, collectively supporting the integrated therapeutic benefits observed. Accordingly, this stage-matched conductive smart hydrogel provides a comprehensive, spatiotemporally controlled strategy for precise post-MI repair. - Source: PubMed
Publication date: 2026/03/12
Song JieFan ZhongxiongBo YakunTaiwaikuli DilareHe JiayuZhang XingJi ShaokaiChen YeminDing HuanhuanWu HetingWang ChaoTang BaopengZhou Xianhui - Th17 cytokines play a central role in the pathophysiology of chronic allergic pulmonary inflammation, influencing multiple signaling pathways that promote inflammation, oxidative stress, and airway remodeling. We evaluated the modulation of the NF-κB, VAChT, and Rho-kinase signaling pathways, and the effects of anti-interleukin (IL)-17 treatment on airway alterations in a murine model of chronic allergic inflammation were exacerbated by lipopolysaccharide (LPS). We studied airway hyperresponsiveness, inflammation, oxidative stress pathways, tissue remodeling, and the expression of various markers in male BALB/c mice with ovalbumin (OVA)-induced chronic allergic inflammation, with or without anti-IL-17 treatment. Twenty-four hours before the end of the experiment, the OVA-sensitized animals were treated with LPS (OVA-LPS-anti-IL-17). Mice treated with OVA-LPS-anti-IL-17 exhibited decreased elastance of the respiratory system after methacholine challenge, along with reduced infiltration of eosinophils, neutrophils, lymphocytes, and macrophages. Anti-IL-17 treatment also reduced the expression of TNF-α, TARC/eotaxin, IL-2, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17, MMP-9, MMP-12, TIMP-1, TGF-β, iNOS, NF-κB, ROCK1, ROCK2, types I and III collagen, decorin, lumican, biglycan, fibronectin, and 8-iso-PGF2α in airway cells, as well as the mRNA expression of IL-17, VAChT, and arginase 1 in lung tissue, compared to the OVA and OVA-LPS groups (P<0.05), except for TNF-α and actin, which were not reduced compared to the OVA group, and Rrs, actin, and VAChT, which were not reduced compared to the OVA-LPS group. Thus, IL-17 blockade helped control bronchial hyperresponsiveness, modulate the IL-17/NF-κB/VAChT/Rho-kinase pathway, suppress chemokine expression, mitigate airway remodeling, and reduce NO-arginase expression in this asthma mouse model with LPS-induced exacerbation. - Source: PubMed
Publication date: 2026/03/30
Camargo L NSantos T M DosSaraiva-Romanholo B MLeick E APrado C MRighetti R FTibério I F L C - DNA methylation (DNAm) is implicated in age-related disease susceptibility. Some studies have reported alterations in DNAm patterns with sleep deprivation, yet this has not been demonstrated in long-term studies. We aimed to analyze whether prolonged mild sleep restriction (SR) results in differentially methylated loci (DML) in selected candidate circadian genes and explore changes in DML epigenome-wide. We conducted a pooled analysis of two randomized crossover trials of SR. Healthy adults (n=60; 65% women, age ≥20y) habitually sleeping 7-9h/night completed two 6-wk (week) intervention periods (condition): maintenance of habitual adequate sleep (AS, ≥7h/night) and SR (-1.5h/night), separated by a washout interval. We determined DNAm levels in morning fasting blood samples collected at baseline and endpoint using EPICv.2 array and multivariable adjusted models for repeated measures and analyzed the sleep condition x week interaction. Pathways and biological processes from the most significant DML were explored. In the candidate core circadian gene approach, sleep condition x week interactions were at cg02394126 (ARNTL; p˂0.001), cg23506964 (CLOCK; p=0.001), cg03701037 and cg06606972 (NPAS2; both p=0.009). In the exploratory EWAS, suggestive top DML were cg23738833 (SNHG3-RCC1; p=1.34E-06), cg13280380 (FAF1; p=2.25E-05), and cg03179866 (MMP12; p=2.78E-05). All but one (cg23738833) showed hypermethylation after SR vs AS. The most significant pathways associated with SR were aging-related genes involved in TGF-beta signaling, glucagon signaling, and fatty acid degradation. These findings reveal that prolonged mild SR is associated with DNAm in core clock candidate genes and suggests DML in other genes across the epigenome suggesting a potentially plastic epigenetic mechanism. Studies are needed to replicate these preliminary findings. - Source: PubMed
Publication date: 2026/03/21
Barragán RocioDye Christian KAggarwal BrookeJelic SanjaColtell OscarCorella DoloresSt-Onge Marie-Pierre