Ask about this productRelated genes to: ICAM1 antibody
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
Related products to: ICAM1 antibody
Related articles to: ICAM1 antibody
- Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated cardioprotective effects in heart failure (HF), yet the molecular mechanisms underlying these benefits remain incompletely understood. This study aimed to characterize cardioprotective effects of SGLT2i, changes of circulating growth and inflammatory factors, as well as adipose tissue gene expression, in subjects with advanced HF (stage D). - Source: PubMed
Publication date: 2026/08/16
Cinkajzlova AnnaKasperova Barbora JuditaIvak PeterNetuka IvanMelenovsky VojtechMrazova Lenka SteinerStranecky ViktorMraz MilosStemberkova Hubackova SonaHaluzik Martin - Long noncoding RNAs (lncRNAs) are key regulators of vascular endothelial function. The lncRNA differentiation antagonizing non-protein coding RNA (DANCR) is implicated in cell proliferation and inflammatory responses; however, its specific role in atherosclerosis remains undefined. - Source: PubMed
Publication date: 2026/08/29
Wang ShutingZhang QiyueLi RongxiaWang YixiaoKamili AdalaitiHan YuqingHou ZhihuiChen YuYang ShujunZhang Weili - Aging is accompanied by an increasing prevalence of frailty and age-related cognitive decline (CD). Cognitive frailty (CF), characterized by physical frailty and cognitive impairment, has been associated with oxidative stress, neuroinflammation, mitochondrial dysfunction, and cardiovascular impairment. However, its biological foundations remain only partially understood. This review synthesizes evidence on biomarkers associated with the blood-brain barrier (BBB) and neurovascular unit (NVU) in CD and CF. These biomarkers are associated with endothelial injury, pericyte damage, BBB permeability, tight junction disruption, glial activation, and extracellular vesicles (EVs). They are assessed by analyzing cerebrospinal fluid (CSF), blood, neuroimaging (including DCE-MRI), and histology. The most frequently evaluated markers were CSF sPDGFRβ, the CSF/serum albumin ratio (QAlb), DCE-MRI permeability, and the adhesion molecules ICAM-1 and VCAM-1. Key convergent findings suggest that BBB breakdown (particularly pericyte injury, as indicated by elevated CSF sPDGFRβ) can precede or occur independently of classical amyloid-β and tau pathology, predict CD in APOE4 carriers over up to 4.5 years, and be associated with disrupted default mode network connectivity. Elevated QAlb demonstrated dose-response prognostic value for clinical deterioration, while DCE-MRI permeability was associated with poorer episodic memory and predicted white-matter injury, which mediated cognitive impairment. Endothelial activation markers were elevated early and predicted progression, whereas vWF exhibited a stage-dependent, potentially biphasic association. Overall, BBB/NVU biomarkers support vascular and neuroinflammatory mechanisms as early, partially Alzheimer's disease-independent contributors to CD and CF, with significant modification by APOE4 and metabolic comorbidities, and with distinct signatures across Alzheimer's disease and vascular cognitive impairment. - Source: PubMed
Publication date: 2026/08/28
Rodríguez-Callejas Juan de DiosMimenza-Alvarado Alberto JoséLomas-Soria ConsueloAguilar-Navarro Sara Gloria - Hyaluronan (HA) is a major glycosaminoglycan of the extracellular matrix that regulates cell migration, signaling, and tissue homeostasis. Its turnover is controlled by coordinated synthesis by HA synthases and degradation by hyaluronidases. Among these hyaluronidases, TMEM2, the only known transmembrane hyaluronidase, plays a unique role in HA degradation at the cell surface; however, the cellular conditions that support its activity remain incompletely understood. To address this, we developed a cell-based HA turnover assay to examine TMEM2-mediated degradation of endogenously synthesized HA, rather than exogenously added, fluorescently labeled HA used in previous studies. Using this system, we show that TMEM2 readily degrades high-molecular weight HA synthesized by co-expressed HAS3. This degradation occurs only when TMEM2 and HAS3 are co-expressed in the same cells (), whereas co-culture of TMEM2-expressing cells with HAS3-expressing cells supports little or no degradation. Interestingly, HA-binding cell surface receptors CD44 and its homolog LYVE-1 promote efficient TMEM2-mediated HA degradation even under conditions, whereas other HA-binding proteins, including TSG-6, layilin, TLR2, RHAMM, and ICAM-1, do not. These findings suggest a spatially regulated mechanism of TMEM2 activity in which capture of HA at the cell surface, mediated by CD44 or LYVE-1, contributes to efficient HA degradation by TMEM2. - Source: PubMed
Publication date: 2026/08/12
Tobisawa YukiYano FumiakiraTomioka-Inagawa RisaIrie FumitoshiKoie TakuyaYamaguchi Yu - : Hydrogen gas (H) inhalation has shown neuroprotective effects in neonatal hypoxic-ischemic models. However, its impact on pulmonary endothelial activation and respiratory function after hypoxic-ischemic insult remains unclear. This study investigated whether H inhalation augments pulmonary endothelial activation or impairs pulmonary function during the acute phase after neonatal hypoxic-ischemic injury. : Sixteen newborn Camborough piglets within 24 h of birth were subjected to hypoxic-ischemic insult and randomized to an untreated group (HI, = 8) or an H-treated group (HI-H, = 8). The HI-H group received 2.1-2.7% H for 6 h. Pulmonary ICAM-1 and inducible nitric oxide synthase (iNOS) expression were assessed by immunofluorescence, lung neutrophils were quantified histologically, and pulmonary function was evaluated using arterial blood gases, oxygen index, and alveolar-arterial oxygen difference. The relationship between lung neutrophil counts and right ventricular cardiac output was also examined. Results: H inhalation did not increase pulmonary ICAM-1 expression or iNOS induction compared with untreated animals. Although lung neutrophil counts were significantly higher in the HI-H group, pulmonary gas exchange remained preserved, with no significant differences in arterial blood gases, oxygen index, or alveolar-arterial oxygen difference. Lung neutrophil counts were positively correlated with right ventricular cardiac output, suggesting that enhanced pulmonary perfusion may contribute to neutrophil redistribution rather than inflammatory recruitment. : H inhalation preserved pulmonary endothelial homeostasis without impairing respiratory function during the acute phase after neonatal hypoxic-ischemic insult. The observed increase in lung neutrophils was not accompanied by evidence of endothelial activation or deterioration of gas exchange, supporting the acute pulmonary safety of H inhalation while suggesting that neutrophil accumulation may, at least in part, reflect hemodynamic redistribution rather than injurious inflammatory infiltration. - Source: PubMed
Publication date: 2026/07/29
Yokota TakayukiIketani MasumiTsuchiya TouiSakamoto KosukeNakao YasuhiroMitsuie TsutomuInoue EriInoue KotaKusaka TomoakiWakabayashi TakayukiKoyano KosukeMiki TakanoriUeno MasakiNakamura ShinjiKusaka Takashi