Ask about this productRelated genes to: MMP12 antibody
- 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 antibody
Related articles to: MMP12 antibody
- 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 - Vitamin D deficiency is associated with poor outcomes and increased mortality in cirrhosis. Calcitriol, the active form of vitamin D3, has antioxidant and hepatoprotective properties; however, its effects on diethylnitrosamine (DEN)-induced liver fibrosis remain unclear. This study investigated the effects of calcitriol on oxidative stress, inflammation, and fibrogenesis in DEN-induced liver fibrosis rat model. Male Sprague-Dawley rats (n = 6/group) were assigned to four groups: control (CON), DEN, DEN + low-dose calcitriol (DEN + LVD3: 5 µg/kg BW), and DEN + high-dose calcitriol (DEN + HVD3: 10 µg/kg BW). Liver fibrosis was induced by weekly DEN injections (70 mg/kg, i.p.) for 8 weeks. Calcitriol was administered twice weekly (i.p.) throughout the experiment. Oxidative stress (hepatic malondialdehyde; MDA), liver injury (serum ALT, AST), hepatic inflammation (NF-κB p65), antioxidant gene expression (SOD-1, GPX-1), and fibrosis markers (TGF-β1, MMP-12, TIMP-1, α-SMA, collagen) were evaluated by biochemical assays, immunohistochemistry, qRT-PCR, western blotting and H&E and Sirius Red staining. Calcitriol significantly attenuated DEN-induced oxidative stress by decreasing hepatic MDA levels in a dose-dependent manner, and lowered serum ALT and AST levels. It partially enhanced hepatic antioxidant defenses by increasing SOD-1 expression toward control levels and upregulating GPX-1 expression. Calcitriol also markedly suppressed NF-κB p65 activation and fibrotic markers (TGF-β1, MMP-12, α-SMA, collagen), which corresponded with improved histopathological fibrosis scores. TIMP1 expression remained unchanged across all groups. Therefore, calcitriol attenuates DEN-induced liver fibrosis by reducing oxidative stress, suppressing inflammatory and fibrogenic signaling, and enhancing antioxidant defenses. - Source: PubMed
Publication date: 2026/05/06
Arramrak KomsanWitayavanitkul NamthipChayanupatkul ManeeratWanpiyarat NatchaSiriviriyakul PrasongWerawatganon Duangporn - Although peripheral artery disease (PAD) is an important diabetes complication, a substantial proportion of cases occur among individuals without diabetes. This study aimed to assess the predictive value of plasma proteomics in the long-term risk of PAD among individuals initially free of diabetes. - Source: PubMed
Publication date: 2026/05/06
Miao Meng-YuanLyu Jie-QiongFang FeiLiu Zhong-YueXu MiaoZhang Hong-JunPan Xing-QiangQin Li-QiangWang Hai-PengChen Guo-Chong - Chronic kidney disease (CKD) is strongly associated with atrial fibrillation. Understanding the biological pathways for this association and creating predictive models has been challenging. Left atrial enlargement is a substrate for atrial fibrillation but any overlap between biomarkers of atrial fibrillation and left atrial enlargement in individuals with CKD is unknown. - Source: PubMed
Publication date: 2026/05/01
Petzl Adrian MRen YueNorby Faye LWang JianqiaoDubin Ruth FAntanavicius IzabeleSegal Mark RChen Lin YeeAlonso AlvaroRhee Eugene PBansal NishaKimmel Paul LVasan Ramachandran SSurapaneni AdityaGrams Morgan EFeldman HaroldMarchlinski Francis EGo Alan SLee HongzheGanz PeterDeo Rajat - Diabetic kidney disease (DKD) is significantly impacting both quality of life and survival rates. The Shen-Yan-Fang-Shuai (SYFS) formula is a traditional Chinese medicine (TCM) compound widely used in the clinical treatment of DKD with proven efficacy, though its potential mechanism of action remains unclear. This study attempts to elucidate the therapeutic efficacy, mechanisms of action, and active compounds of the SYFS formula in the treatment of DKD. - Source: PubMed
Kang YiJin QianZhou MengqiZheng HuijuanLi DanwenWang XuezheZhou JingweiLv JieWang Yaoxian