Ask about this productRelated genes to: CD106 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: CD106 antibody
Related articles to: CD106 antibody
- Endothelial dysfunction characterized by cytokine release and adhesion molecule upregulation is a major driver of atherogenesis. Tumor necrosis factor-α (TNF-α) activates NF-κB signaling and increases ICAM-1, VCAM-1, IL-6, and IL-8 expression in endothelial cells. This study aimed to investigate whether amentoflavone (AMF) modulates TNF-α-induced inflammatory and adhesion-related responses in human endothelial cells, supporting its potential to mitigate early vascular dysfunction. - Source: PubMed
Publication date: 2026/04/30
Turk Fatih CanOnal BurakCelik ZulalAkkan Ahmet GökhanÖzyazgan Sibel - Protein epigenetic scores (EpiScores) are DNA methylation (DNAm)-based proxies for circulating protein levels and may provide insights into inflammation-cognition relationships. Although some EpiScores have been linked to cognitive decline, it remains unclear whether these proxies show similar associations in other cohorts, and whether their effects vary across distinct cognitive domains. We aimed to evaluate the associations between inflammatory proteins EpiScores and cognitive functions including specific domains in the Swedish Adoption/Twin Study of Aging (SATSA) cohort. We analyzed 1332 repeated measurements from 520 SATSA participants across up to six testing waves (1992-2014). Inflammatory protein EpiScores (N = 27) were generated using previously published CpG site-specific weights. Outcomes were a global cognitive function (GCF) score and four specific cognitive domains (verbal ability, spatial ability, memory, and perceptual speed). We applied marginal linear models within the generalized estimating equations (GEE) framework to estimate population-averaged longitudinal associations, controlling the false discovery rate (FDR) using the Benjamini-Hochberg (BH) procedure (q < 0.05 considered significant). Two EpiScores-C-X-C motif chemokine ligand 9 (CXCL9) and vascular cell adhesion molecule 1 (VCAM1)-showed significant positive associations with GCF. In domain-specific outcomes, VCAM1 demonstrated a positive association with spatial ability, whereas C-X-C motif chemokine ligand 11 (CXCL11) had a negative association with verbal ability. These associations were broadly consistent across multiple sensitivity analyses. Inflammation-related DNAm signatures of certain proteins were associated with cognitive performance in SATSA samples. Moreover, the associations differ by cognitive domain. Future longitudinal studies are warranted to clarify the causal implications of these EpiScore-cognition associations and to explore population differences in DNAm patterns. - Source: PubMed
Publication date: 2026/04/30
Ishihara KazuyukiHägg SaraLopes De Oliveira Thaís - Vascular endothelial inflammation is a key pathological process underlying various inflammatory vascular conditions, which can lead to severe cardiovascular complications. Shexiang Tongxin Dropping Pills (STDP) is a traditional Chinese medicine formulation clinically used for cardiovascular disorders and has shown protective effects on the vascular endothelium. However, the specific mechanisms by which STDP attenuates vascular endothelial inflammation remain incompletely elucidated. - Source: PubMed
Publication date: 2026/04/29
Liu JingyaWang KeYou HongjingLong LiangXu YueChen QiuheChen Yang - Steroid-refractory acute graft-versus-host disease (SR-aGVHD) is a severe complication of allogeneic hematopoietic cell transplantation. While endothelial dysfunction is implicated in aGVHD pathophysiology, the status of the endothelium in patients with SR-aGVHD and the effect of the JAK1/2 inhibitor ruxolitinib at the microvascular level remain incompletely understood. This study aimed to characterize the endothelial damage phenotype induced by SR-aGVHD serum and to evaluate the potential modulatory effects of ruxolitinib. Human microvascular endothelial cells (HMEC-1) were exposed to serum from SR-aGVHD patients (n=21) or healthy donors (C), with or without ruxolitinib (0.4 µM). Markers of endothelial activation (VCAM-1, ICAM-1), junctional integrity (VE-cadherin), prothrombotic state (VWF), apoptosis (cleaved caspase-3), and intracellular signalling (JAK-STAT and MAPK families) were analyzed by immunofluorescence and immunoblotting. Compared with C, SR-aGVHD serum caused increased VCAM-1 and ICAM-1 expression (p<0.05 for both), reduced VE-cadherin (p<0.01), elevated VWF production, and cleaved caspase-3 presence (p<0.05 for both). These changes were associated with significant phosphorylation of STAT3 (p<0.05), STAT1 (p<0.05), and key MAPK proteins (Erk1/2, p38, SAP/JNK, and cJun) (p<0.05, all). Ruxolitinib treatment effectively mitigated these responses, reducing adhesion molecule expression, restoring VE-cadherin localization, normalizing VWF production, and suppressing apoptosis. These protective effects were associated with a significant inhibition of the activated JAK-STAT and MAPK signalling pathways. SR-aGVHD serum directly induces endothelial activation in vitro, promoting a pro-inflammatory and prothrombotic phenotype. Ruxolitinib counteracts these effects, demonstrating a direct endothelial-protective role via suppression of JAK-STAT and MAPK signalling. These findings provide a novel mechanistic insight into its therapeutic efficacy in SR-aGVHD. - Source: PubMed
Publication date: 2026/04/28
De Moner BlancaMartinez-Sanchez JuliaEscribano-Serrat SilviaMoreno-Castaño Ana BelenCharry PaolaCid JoanLozano MiquelArellano-Rodrigo EduardoSalas Maria QueraltRovira MontserratMartinez CarmenEscolar GinesCarreras EnricÁlvarez-Larrán AlbertoDiaz-Ricart Maribel - Systemic inflammation presents a significant challenge to the long-term function of biohybrid implants. While endothelialisation of biohybrid implants has been shown to improve device hemocompatibility, its feasibility under the influence of patients' inflammatory status remains largely unexplored. To investigate this, we developed a controlled in vitro model which allows to study endothelial dysfunction under inflammatory stress. - Source: PubMed
Publication date: 2026/04/09
Cheremkhina MariaBabendreyer AaronNeullens Christopher TKrapp SusannePabst AlessaOhl KimRuetten StephanLudwig AndreasCornelissen Christian GJockenhoevel StefanTenbrock KlausThiebes Anja Lena