Ask about this productRelated genes to: ICAM1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: ICAM1 Blocking Peptide
- CD44 is a cell-surface glycoprotein frequently overexpressed in cancers and associated with poor prognosis. We evaluated the prognostic significance of CD44 overexpression in multiple myeloma (MM) and investigated the therapeutic efficacy of combining natural killer (NK) cell therapy with all-trans retinoic acid (ATRA) and bortezomib (Bor) against CD44-overexpressing MM. Clinical data from the CoMMpass database were analyzed to assess survival outcomes relative to CD44 expression. NK cells were expanded from healthy donors using K562-OX40L-mbIL-18/21 feeder cells supplemented with interleukin (IL)-2 and IL-15. Functional assays were performed using CD44-high myeloma cell lines treated with ATRA and Bor, individually or in combination with NK cells. Therapeutic efficacy was evaluated based on tumor growth, systemic dissemination, and survival in an intravenous U266-green fluorescent protein-firefly luciferase xenograft NOD/SCID IL-2Rγnull mouse model. Clinical data showed CD44 overexpression correlated with inferior overall survival (P < 0.0001) in all three stages I, II, and III of the revised International Stage System. In vitro, ATRA and Bor co-treatment downregulated β-catenin and CD44 expression, inhibited proliferation, migration, and invasion, and enhanced NK cell-mediated cytotoxicity via upregulation of MICA/B, Fas, TRAIL-R2, and intercellular adhesion molecule-1. In vivo, combination therapy with NK cells, ATRA, and Bor significantly suppressed CD44 expression, reduced extramedullary spread, and prolonged survival without notable toxicity. These preclinical findings support CD44 overexpression as a marker associated with inferior survival in MM and provide a rationale for pharmacologic tumor priming with ATRA and bortezomib to enhance NK cell-mediated cytotoxicity. However, the therapeutic strategy requires further validation in heterogeneous patient-derived models and prospective clinical studies before clinical efficacy can be inferred. - Source: PubMed
Publication date: 2026/05/21
Nguyen Van-TanThi Thuy NguyenTran Van-Dinh-HuanVo Manh-CuongChu Tan-HuyJang Ho CheolKim MiheeSong Ga-YoungAhn Seo-YeonAhn Jae-SookYang Deok-HwanKim Hyeoung-JoonCho DuckLee ChanghoJung Sung-HoonLee Je-Jung - Calcium (Ca), iron (Fe), and copper (Cu) during pregnancy may have both cardiovascular protective and risk effects, but their dose-response relationship is still unclear. - Source: PubMed
Publication date: 2026/05/19
Wang XiangdongZhang LeiWang XuehaiZu PingPan RubinWang PengChen XianxiaJiang PinChen JiexiaZhu Peng - Crimean-Congo hemorrhagic fever virus (CCHFV) is a highly pathogenic tick-borne bunyavirus. Infection and dysfunction of the vascular endothelium are likely key factors in CCHFV pathogenesis, yet the underlying mechanisms remain poorly understood. Using a mouse model, we demonstrated that CCHFV directly infects vascular endothelium, leading to marked activation and damage, as evidenced by the upregulation of adhesion molecules. To further investigate this phenomenon, we performed a quantitative proteomics study on CCHFV-infected human umbilical vein endothelial cells (HUVECs), confirming a significant upregulation of cell adhesion molecular pathways. Notably, the key adhesion molecule intercellular adhesion molecule 1 (ICAM-1) was prominently induced upon infection, which was transcriptionally dependent on NF-κB. ICAM-1 interacts with its receptor integrin (LFA-1) on leukocytes to mediate firm adhesion and transmigration, thereby driving inflammatory responses. Using an established adhesion assay, we found that CCHFV infection robustly increased the adhesion of Jurkat T cells to HUVECs. This enhanced adhesion was specifically dependent on ICAM-1, as it was substantially reduced by knockdown of or by competition with its soluble extracellular domain. Moreover, lifitegrast-an approved anti-inflammatory small-molecule antagonist that selectively blocks ICAM-1/LFA-1 interaction, significantly inhibited CCHFV-induced Jurkat T cell adhesion. Importantly, in a lethal murine model of CCHFV infection, the treatment with lifitegrast sodium improved survival rates and concurrently alleviated leukocyte infiltration and tissue damage. These findings delineate an ICAM-1-mediated mechanism of vascular activation and inflammation in CCHFV infection and highlight a promising anti-inflammatory-based strategy for treating CCHF. - Source: PubMed
Publication date: 2026/04/30
Liu YajieLi LiushuaiLiu KaiChen ShuoWu FanLi JiangZhou XinboHu ZhihongZhong WuWang Manli - Metabolic syndrome (MetS) definitions may perform differently in indigenous populations with distinct genetic and lifestyle exposures. The Negrito community remains under-represented in cardiometabolic research despite emerging risk. Building on earlier observations of atypical biomarker patterns in this population, potentially linked to CDH13-related vascular mechanisms, this study aimed to determine MetS prevalence using the International Diabetes Federation (IDF) and Harmonized Joint Interim Statement (JIS) definitions, evaluate agreement between these definitions and their concordance with cardiovascular risk scores (CRS), and examine relationships between inflammatory and vascular biomarkers in the context of MetS. A cross-sectional study was conducted among Negrito adults. MetS was categorized using the IDF and JIS definitions. CRS included the Framingham risk score (FRS), Castelli risk index (CRI)-I, CRI-II and the atherogenic index of plasma (AIP). High-sensitivity C-reactive protein, lipoprotein(a), soluble intercellular adhesion molecule-1 (sICAM-1), and T-cadherin were quantified. Agreement statistics, correlations, logistic and linear regression models were applied. Among 153 adults, MetS prevalence was 11.8% (IDF) and 16.3% (JIS) with near-perfect agreement (κ = 0.81), although McNemar testing indicated slight asymmetry between definitions. Concordance between MetS and CRS was generally weak, with AIP showing the highest agreement (IDF κ = 0.17; JIS κ = 0.30), followed by CRI-II (IDF κ = 0.05; JIS κ = 0.20). CRI-I showed slight agreement with both definitions (IDF κ = 0.07; JIS κ = 0.15), while FRS showed no meaningful alignment (IDF κ = -0.07; JIS κ = -0.01). sICAM-1 showed weak but consistent positive correlations with all CRS (r = 0.20-0.26, P = .017-.002). T-cadherin did not correlate with CRS but was inversely associated with sICAM-1 (r = -0.28, P = .001). In multivariable logistic models, CRI-I (OR = 3.20), CRI-II (OR = 2.32) and AIP (OR = 2.15) remained independently associated with MetS. In linear models, sICAM-1 showed consistent associations with each CRS (FRS R2 = 0.03; CRI-I R2 = 0.06; CRI-II R2 = 0.06; AIP R2 = 0.03). IDF and JIS definitions classified MetS similarly but showed limited concordance with CRS. AIP and CRI demonstrated stronger cross-sectional associations with MetS than FRS. Biomarker analyses indicated that sICAM-1 correlated with CRS. The inverse relationship between T-cadherin and sICAM-1 raises the possibility of compensatory vascular-protective mechanisms. Collectively, these findings suggest a distinct lipid-inflammatory cardiometabolic phenotype in the Negrito population, where endothelial activation markers may capture early vascular stress beyond traditional risk scores. - Source: PubMed
Mokhsin AtiqahFaisal Andrian AlifOthman Noor Mohd FirdausOthman Nor'AshikinMohd Ismail AletzaChen Xin WeeHoh Boon-PengAbdul Rahman Thuhairah - Extracellular vesicles (EVs) contribute to stroke rehabilitation by mediating intercellular signaling during inflammation and tissue repair. Here we report EV-associated surface proteins as potential biomarkers for predicting recovery of activities of daily living (ADL) during the subacute phase of ischemic stroke (IS). IS patients and healthy controls (HCs) were recruited for this study, with serum samples analyzed across three study stages. In the discovery subset (10 IS, 6 HCs), serum proteomics was used to identify differentially expressed proteins (DEPros) and perform Gene Ontology (GO) enrichment analysis. In the exploration subset (7 IS, 12 HCs), a proximity-dependent barcoding assay (PBA) was employed to profile surface proteins on individual EVs and screen for biomarker candidates. In a validation cohort, patients were grouped by ADL improvement (little-effect recovery, LE, = 30; obvious-effect recovery group, OE, = 22) based on Longshi Scale and Barthel Index assessments at admission and at 3 months follow-up. Targeted biomarker validation was performed with enzyme-linked immunosorbent assay (ELISA) and receiver operating characteristic (ROC) analysis. A total of 113 DEPros were identified, with GO term enrichment in EV-related pathways. PBA profiling revealed matrix metalloproteinase 9 (MMP9), carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), melanoma cell adhesion molecule (MCAM), and gelsolin (GSN) as candidate biomarkers. In the validation cohort, MMP9 and CEACAM1 were significantly elevated in the LE group. ROC analysis showed area under the curve (AUC) of 0.726 for MMP9 and 0.700 for CEACAM1 in distinguishing LE from OE. Elevated serum levels of EV-associated biomarkers MMP9 and CEACAM1 were associated with poor ADL recovery, supporting their potential as prognostic biomarkers for stroke rehabilitation outcomes. - Source: PubMed
Publication date: 2026/04/13
Luo JiaoCai YouCai YanlingZhang ChunxiaLiu AnkangHuo YongyangFan XuehuiYe RuixueGao HongHuang MeilingZhang XiaohuaZhou MingchaoWang Yulong