MMP_8 catalytic domain, human, 13C, 15N
- Known as:
- MMP_8 catalytic domain, H. sapiens, 13C, 15N
- Catalog number:
- 1010008C_CN
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- MMP_8 catalytic domain human 13C 15N
Related genes to: MMP_8 catalytic domain, human, 13C, 15N
- Gene:
- MMP8 NIH gene
- Name:
- matrix metallopeptidase 8
- Previous symbol:
- CLG1
- Synonyms:
- -
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-11
- Date modifiied:
- 2015-08-25
Related products to: MMP_8 catalytic domain, human, 13C, 15N
Related articles to: MMP_8 catalytic domain, human, 13C, 15N
- Peripheral artery disease (PAD) confers elevated risk for major adverse cardiovascular events (MACE), yet accurate risk stratification remains a challenge, particularly among patients with advanced disease necessitating endovascular revascularization. This study aimed to improve the prediction of MACE in a clearly defined high-risk PAD population (hospitalized patients undergoing endovascular intervention) by identifying novel protein biomarkers and developing a robust risk model. We prospectively analyzed blood samples from 164 hospitalized PAD patients scheduled for endovascular revascularization, employing untargeted plasma proteomics and metabolomics. Differential protein and metabolite profiles were compared between patients with and without subsequent MACE. Several proteins, including MMP3, MMP19, and PRB2, were markedly elevated in patients who developed MACE. A proteomics-based risk model incorporating these biomarkers achieved high discriminative accuracy (area under the curve > 0.80) for identifying individuals at increased risk. Metabolomic profiling revealed additional pathway alterations, notably involving tryptophan and glycogen metabolism, which provided mechanistic insights into cardiovascular complications but were not directly incorporated into the prediction model. This study demonstrates that integrating protein biomarkers markedly improves risk stratification in advanced PAD patients undergoing surgical intervention. The findings offer promising tools for early detection and enable more personalized management for this high-risk subgroup, while also deepening understanding of disease pathophysiology. However, further validation in larger and more diverse prospective cohorts is warranted before these findings can be broadly applied in clinical practice. - Source: PubMed
Publication date: 2026/05/06
Zhao WenxinMeng LingbingYan ShengLi PengSun YoujingGuo YamingZhang BowenCao Yifan Ren JunhongLi YongjunChen Zuoguan - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard - Acute coronary syndrome (ACS) and ischemic stroke are major life-threatening conditions caused by atherosclerosis. Although the mechanisms of atherosclerosis appear to be broadly similar across different vascular beds, growing evidence suggests that there are morphological and histological differences between coronary and carotid atherosclerosis. To identify disease-specific therapeutic strategies, we aimed to compare ACS and chronic coronary syndrome (CCS) in coronary artery disease, and symptomatic and asymptomatic carotid artery disease. - Source: PubMed
Publication date: 2026/03/17
Yoshida TakeshiEmoto TakuoYamamoto HiroyukiTakaya TomofumiSawada TakahiroMurphy Sarah LouiseShoda MitsuhikoNakamura KeisukeTaniguchi MasayukiSasaki NaotoFukuishi YutaToba TakayoshiOhkawa TakenaoFuruyashiki TomoyukiKawai HiroyaHirata Ken-IchiOtake HiromasaYamashita Tomoya - Matrix metalloproteinase (MMP) expression and function are highly context dependent, varying across physiological and pathological conditions. We previously documented the expression profiles of select MMPs in the ischemic brains of young male rodents. However, aging is a major risk factor for stroke in humans and is associated with vasculature alterations, increased oxidative stress, and elevated inflammation. In addition, sex differences have been reported in stroke incidence and severity. Despite this, the effects of age, sex, and species on brain MMP gene expression after cerebral ischemia/reperfusion (I/R) has not been systematically examined. Therefore, we investigated how age, sex, and species influence the mRNA expression of all known MMPs (22 total) in the brain following cerebral I/R. Moderate-to-severe neurological deficits were induced by transient middle cerebral artery occlusion (MCAO) followed by reperfusion in young and aged male and female C57BL/6 mice and in young male Sprague-Dawley rats. Brain tissue from the ipsilateral (ischemic) hemisphere was collected on post-MCAO day 1, and MMP mRNA levels were quantified by real-time PCR and expressed as fold change relative to the sham control group. Across species, MMP-3, MMP-8, MMP-12, MMP-13, MMP-19, MMP-20, and MMP-27 were upregulated in both rats and mice. Species-specific increases were also observed: MMP-1, MMP-7, MMP-9, MMP-14, MMP-21, and MMP-25 were upregulated only in rats, whereas MMP-10 was upregulated only in mice. The most strongly upregulated MMPs were MMP-12 in rats and MMP-3, MMP-10, and MMP-12 in mice. By contrast, MMP-15 and MMP-17 were downregulated in both species, whereas MMP-23 and MMP-24 were downregulated only in rats and mice, respectively. Within mice, MMP-3, MMP-10, MMP-12, MMP-19, MMP-20, and MMP-21 increased in both sexes and age groups, except for MMP-19 in aged males and MMP-21 in young males. MMP-14 increased only in females (young and aged), whereas MMP-27 increased only in males (young and aged). Notably, MMP-3, MMP-10, and MMP-12 were the three most highly upregulated MMPs in both male and female mice regardless of age. Overall MMP mRNA expression levels were higher in aged male mice and lower in aged female mice relative to sex-matched young mice. Among all MMPs examined, MMP-12 showed the most marked upregulation across species and, within mice, across age groups and sexes. Collectively, these findings demonstrate that brain MMP gene expression after cerebral I/R is modulated by age, sex, and species, underscoring the importance of incorporating these biological variables when targeting MMPs individually or in combination in preclinical rodent stroke models. - Source: PubMed
Publication date: 2026/02/26
Challa Siva ReddyBaker Isidra MVinayagam VisheshJackson Samantha NKhan NabeehaMada Sahil ReddyUnnam PavaniFornal Casimir AKlopfenstein Jeffrey DVeeravalli Krishna Kumar - To characterize clinical and transcriptomic differences in juvenile scleromyositis overlap (jOverlap) compared to juvenile systemic sclerosis (jSSc) and juvenile dermatomyositis (JDM), focusing on autoantibody profiles, organ involvement, treatment, and peripheral blood gene expression. - Source: PubMed
Robinson Amanda DPain Clare EMorgan Gabrielle ASanyal AnweshaChaparala SrilakshmiPachman Lauren MTorok Kathryn S