TACE Antibody
- Known as:
- TACE Antibody
- Catalog number:
- 1131
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TACE Antibody
Related genes to: TACE Antibody
- Gene:
- ADAM17 NIH gene
- Name:
- ADAM metallopeptidase domain 17
- Previous symbol:
- TACE
- Synonyms:
- cSVP, CD156B
- Chromosome:
- 2p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2019-04-23
Related products to: TACE Antibody
Related articles to: TACE Antibody
- Liver fibrosis is a progressive pathological condition closely linked to gut microbiota dysbiosis and impaired intestinal barrier integrity. Vildagliptin, a dipeptidyl peptidase-4 inhibitor used in type 2 diabetes, exhibits pleiotropic anti-inflammatory and antioxidant properties; however, its impact on the gut-liver axis during hepatic fibrogenesis remains insufficiently defined. This experimental study investigated whether concomitant vildagliptin administration attenuates the development of CCl₄-induced liver fibrosis and whether this effect is associated with alteration in gut microbial composition, intestinal barrier-related markers, and circulating lipopolysaccharide (LPS), and hepatic fibrosis-associated molecular changes. Male rats were allocated to five groups: normal control, Vildagliptin alone (20 mg/kg/day), CCl₄-fibrosis, and CCl₄ + Vildagliptin (10 or 20 mg/kg/day). Liver fibrosis was induced by CCl₄ administration for six weeks, with concomitant daily oral Vildagliptin in the treatment groups. Liver function indices, fibrotic markers, oxidative stress parameters, and serum LPS were assessed. Intestinal barrier-related changes were assessed by measuring colonic ZO-1 and occludin levels, while circulating LPS was quantified as a marker of systemic endotoxemia. Hepatic ADAM17, Notch-1, DNMT3A, and Smad7 protein levels and β-Klotho mRNA expression were assessed. Liver and colon histopathology was examined, and gut microbiota composition was profiled using 16S rRNA gene amplicon sequencing. Vildagliptin significantly ameliorated CCl₄-induced liver injury and fibrosis, evidenced by improved biochemical parameters, reduced collagen deposition and hydroxyproline, and attenuation of hepatic stellate cell activation. These effects were accompanied by increased colonic ZO-1 and occludin levels, reduced circulating LPS, decreased hepatic ADAM17, Notch-1, and DNMT3A protein levels, increased β-Klotho mRNA expression and Smad7 protein levels, and alterations in gut microbiota composition. Collectively, concomitant vildagliptin administration attenuated the development of CCl₄-induced liver fibrosis and was associated with modulation of gut-liver axis -related changes and alterations in LPS- and Notch-related molecular markers. - Source: PubMed
Publication date: 2026/10/01
Eid Aya MEl-Gendy Ahmed OEwees Mohamed Gamal El-Din - Acute respiratory distress syndrome (ARDS) is characterized by endothelial barrier disruption, excessive neutrophil recruitment, and sustained pulmonary inflammation. The A Disintegrin and Metalloproteinase 17 (ADAM17) regulates inflammatory signaling through ectodomain shedding of adhesion molecules and cytokine receptors, yet its endothelial-specific contribution to acute lung injury remains poorly defined. - Source: PubMed
Publication date: 2026/09/28
Biedritzky AnnaKleinmaier CarolinFuhr AnikaHerrmann Lisa MariaNgamsri Kristian-ChristosKonrad FranziskaKoeppen Michael - Respiratory syncytial virus (RSV) infection causes epithelial injury, barrier disruption, and formation of syncytia in human lung tissue; however, the regulatory host defense mechanisms involved remain poorly defined. ADAM17 is a multifunctional sheddase implicated in inflammatory lung disease and is considered a potential therapeutic target during viral infections. Here, we show that RSV infection induces ADAM17 activity through PKC- and ERK-dependent signaling, increasing surface ADAM17 levels and sheddase activity. Genetic loss or pharmacological inhibition of ADAM17 reduced RSV-induced formation of syncytia, post-entry viral spread, and viral titers. This identifies ADAM17 as a host factor that supports viral dissemination. ADAM17 deficiency simultaneously exacerbated RSV-induced epithelial injury, characterized by loss of intercellular cohesion, impaired barrier function, increased paracellular permeability, and enhanced cytotoxicity. RSV-induced ADAM17 activity promoted the release of multiple epithelial growth factor receptor (EGFR) ligands. Supplementation with recombinant amphiregulin partially restored barrier function in infected ADAM17-deficient cells. Consistent with these functional effects, ADAM17 deficiency was associated with the loss of epithelial differentiation-associated transcriptional programs and increased expression of inflammatory genes. These findings indicate that ADAM17 plays a dual role in RSV infection. It facilitates syncytial viral spread, while preserving epithelial integrity through autocrine EGFR signaling. Thus, ADAM17 activity represents a biological trade-off between viral dissemination and tissue protection, indicating that therapeutic ADAM17 inhibition may reduce viral spread at the cost of aggravating epithelial damage.IMPORTANCEDuring respiratory syncytial virus (RSV) infection, the airway epithelium must maintain barrier integrity while responding to virus-induced syncytium formation and tissue damage. It is poorly understood which host factors balance tissue preservation against viral replication and spread. Here, we demonstrate that the host cellular metalloproteinase ADAM17 is activated upon RSV infection. While RSV-induced ADAM17 activity promotes syncytium formation and viral spread, it concurrently controls the maintenance of epithelial barrier integrity, preserves cell survival, and inhibits hyperinflammatory signaling. By demonstrating that ADAM17 has a dual mode of action controlling both viral propagation and epithelial barrier resilience, this work uncovers a central trade-off: the same host factor exploited by RSV for dissemination is essential for protecting airway tissue. Consequently, targeting ADAM17 for antiviral therapy presents major challenges, as blocking viral spread may compromise vital epithelial defenses. - Source: PubMed
Publication date: 2026/09/28
Meineke RobertKnittler Marie-ChristinTagore RajarsheeEngling NeleLudlow MartinOsterhaus Albert D M ERimmelzwaan Guus F - Anastomotic leakage continues to be a severe and prevalent complication in colorectal surgery, leading to elevated morbidity and mortality rates despite modern advancements in surgical and perioperative care. To address this persistent clinical challenge, the aim of the present study was to engineer a biocompatible poly(lactic-co-glycolic acid) (PLGA) matrix designed for the sustained release of melatonin, subsequently evaluating its therapeutic efficacy in promoting colon anastomotic repair. Seventy-two male Wistar albino rats were randomly assigned to three experimental groups: anastomosis (n = 24); anastomosis + matrix (n = 24); and anastomosis + melatonin-loaded matrix (n = 24). Anastomotic segments were harvested on postoperative days 3 and 7, and colonic bursting pressure was measured as a functional indicator of anastomotic integrity. The melatonin-loaded matrix significantly enhanced anastomotic healing on postoperative day 7. Melatonin delivery: (1) markedly reduced the gene expression of pro-inflammatory cytokines; (2) modulated iNOS, COX-2 and MPO expression on both days 3 and 7; (3) decreased HO-1 and catalase expression on day 7; (4) promoted collagen synthesis; (5) enhanced collagen deposition through upregulation of Arg-1; and (6) regulated ADAM10 and ADAM17 gene expression. These results are correlated with the histological analysis findings. Collectively, controlled release of melatonin via a PLGA-based biomaterial matrix promotes colon anastomosis healing. This strategy represents a promising translational approach for reducing postoperative anastomotic complications. - Source: PubMed
Publication date: 2026/09/27
Demir UfukYurtgezen Zekiye GülfemErbil GülfemGökçe Oruç NumanOral AyhanUzun Metehan - Cardiopulmonary bypass (CPB) alters blood flow patterns and may induce endothelial activation; however, the effects of different CPB configurations on endothelial-associated biomarkers remain unclear. In this exploratory pilot study, we compared circulating biomarkers and tissue immunohistochemical findings between beating-heart partial CPB and cardioplegic total CPB in juvenile pigs. Ten 8-week-old female crossbred piglets underwent partial CPB with continued cardiac beating ( = 5) or total CPB with aortic cross-clamping and cardioplegic arrest ( = 5) for 60 min. Serum vascular cell adhesion molecule-1 (VCAM-1), a disintegrin and metalloproteinase-17 (ADAM-17), and thrombospondin-1 (TSP-1) concentrations were measured using an enzyme-linked immunosorbent assay, and tissue VCAM-1 and platelet endothelial cell adhesion molecule-1 (PECAM-1) were assessed immunohistochemically. At the end of the CPB procedure, serum VCAM-1 was higher in the total CPB group than in the partial CPB group (581 [339-759] ng/mL vs. 239 [224-304] ng/mL; |rank-biserial r| = 0.84 (95%CI, 0.36 to 1.00); Hodges-Lehmann estimate of the location shift = 341.7 ng/mL, 95% CI, 5.1-607.0 ng/mL; = 0.03), whereas ADAM-17 and TSP-1 and tissue findings showed no consistent intergroup differences. Total CPB was associated with an early increase in circulating VCAM-1. Because the CPB configurations differed in several physiological and procedural factors, this response should be interpreted as configuration-associated rather than as evidence of an isolated effect of reduced pulsatility. - Source: PubMed
Publication date: 2026/08/25
Udagawa HiromuHamamoto YujiNam EunryelOkamoto MinoruKomatsu MasafumiIsaka Mitsuhiro