VCAM1 Antibody
- Known as:
- VCAM1 Antibody
- Catalog number:
- abx000664
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- VCAM1 Antibody
Related genes to: VCAM1 Antibody
- Gene:
- VCAM1 NIH gene
- Name:
- vascular cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- CD106
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2016-10-05
Related products to: VCAM1 Antibody
Related articles to: VCAM1 Antibody
- Circulating biomarkers reflecting inflammation and endothelial dysfunction have been proposed as indicators of cerebral small vessel disease; however, their relevance during the hyperacute phase of ischemic stroke remains uncertain. We aimed to determine whether circulating biomarkers measured on admission differ between small ischemic stroke subtypes and whether they provide prognostic information beyond conventional predictors. We conducted a retrospective analysis of 168 patients with acute ischemic stroke treated with intravenous thrombolysis within 4.5 h of onset, classified by MRI as having recent small subcortical infarcts (RSSI; n = 84) or small cortical or cortico-subcortical infarcts (non-RSSI; n = 84). We measured admission blood levels of interleukin-1β, interleukin-6, matrix metalloproteinase-9 (MMP-9), vascular cell adhesion molecule-1 (VCAM-1), neurofilament light chain (NfL), C-reactive protein (CRP), and leukocyte ratios, and evaluated their associations with 3‑month functional outcomes using the modified Rankin Scale. Our findings showed that RSSI patients were younger (66 vs. 74 years, p < 0.001) and had smaller infarcts (0.68 vs. 2.55 mL, p < 0.001). Higher NfL (OR 2.07, p < 0.001) and VCAM‑1 levels (OR 1.84, p = 0.034) were associated with poorer outcomes. Notably, the prognostic contribution of CRP, MMP‑9, and VCAM‑1 was more pronounced in patients with RSSI. These findings suggest that circulating biomarkers may offer additional prognostic value, with patterns varying across small ischemic stroke subtypes, though their clinical utility warrants further investigation. - Source: PubMed
Publication date: 2026/05/18
Ramis DarioRudilosso SalvatoreGirona AndresBrengaret OnaRosa-Batlle IreneCabero-Arnold AndreaVargas MarthaBartolome-Arenas InesDoncel-Moriano AntonioRodriguez-Vazquez AlejandroLlull LauraRenu ArturoUrra XabierAmaro SergioChamorro Angel - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Diabetic cardiomyopathy (DCM) involves progressive cardiac dysfunction driven by vascular endothelial injury and cellular senescence. However, precisely targeting pre-senescent cells remains a major therapeutic challenge. Herein, through single-cell RNA sequencing of diabetic mouse hearts, we identified VCAM1 -positive (VCAM1) cells as a distinct pre-senescent endothelial population. Both scRNA-seq and subsequent immunofluorescence analyses confirmed the concurrent upregulation of cGAS-STING signaling within this VCAM1 population, nominating it as a critical therapeutic target for early intervention. To specifically deliver a STING antagonist to these cells, we developed a biomimetic delivery platform based on engineered HEK293T cell-derived nanovesicles. Through lipidomic analysis, we reprogrammed the vesicle membrane composition to mimic that of endothelial cells, thereby creating nanovesicles with enhanced membrane fusogenic properties (F-NVs). After loading with H151, a potent STING pathway inhibitor that acts by inhibiting STING phosphorylation, the resulting F-NVs-tVCAM1@H151 efficiently targeted VCAM1 pre-senescent cells, potently inhibited their transition into a senescent state, and significantly reduced the overall senescent burden in the diabetic heart. Consequently, this targeted strategy alleviated cardiac microvascular injury and markedly improved cardiac function in diabetic mice. This work identifies VCAM1 as a novel pre-senescent marker and demonstrates membrane lipid engineering as an effective approach for targeted nanovesicle delivery, offering a precise targeted therapeutic paradigm for DCM. - Source: PubMed
Publication date: 2026/05/17
Liu YangLiang ShuangBu FanWu PengyingZhou XueyingZhao JingShen MingzhiWei MengyingYang GuodongYuan Lijun - Advanced glycation end products (AGEs), particularly AGE-modified albumin (AGE-BSA), have been implicated in vascular inflammation and endothelial dysfunction, while neutrophil extracellular traps (NETs) are known to aggravate endothelial injury. Here, we investigated whether AGE-BSA directly promotes endothelial inflammatory and thrombotic activation, modulates neutrophil oxidative stress and NET formation, and may enhance NET-induced endothelial inflammation. - Source: PubMed
Publication date: 2026/05/15
Junho Carolina Victoria CruzDai YusangSchieren LuisaHourtz SinaRykova TetianaVondenhoff SonjaWessiepe MartinaZou JinmiJankowski JoachimGoettsch ClaudiaNoels Heidi - Alzheimer's disease (AD) is a progressive neurological disorder associated with high prevalence. Numerous studies have been conducted to regulate the expression of inflammatory genes, indicating that any changes may ultimately lead the nervous system toward disease pathogenesis. ANXA1, VCAM1, and CCL2 are among the genes involved in immune and inflammatory pathways. In this study, we aim to examine their expression in individuals with Alzheimer's disease and healthy individuals using bioinformatics and laboratory methods. - Source: PubMed
Publication date: 2026/05/16
Fattahi FatemeAbed SaminKouchakali GhazalDerakhshan Sima MansooriSadeh Reza NaghdiKhaniani Mahmoud Shekari