| 1991 |
The human VCAM1 gene is organized into 9 exons spanning ~25 kb, with exons 2–8 encoding C2/H-type immunoglobulin domains. Alternative mRNA splicing that includes or excludes exon 5 generates at least two different VCAM-1 precursor isoforms. The promoter contains NF-κB, GATA family, and AP1 consensus binding sites, and the gene maps to chromosomal region 1p31–32. |
Genomic cloning, exon mapping, Southern blot, in situ hybridization, human-mouse hybrid cell line analysis, promoter sequence analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
1715583
|
| 1993 |
The murine VCAM1 gene contains 10 exons spanning ~20 kb. Alternative splicing of exon 5 generates a truncated three-Ig-domain isoform linked to the membrane via a phosphatidylinositol anchor (encoded by exon 5), distinct from the full-length transmembrane form. The murine core promoter shares conserved NF-κB, Ets, and GATA transcription factor binding sites with the human gene. |
Genomic cloning, exon mapping, sequence analysis of promoter and splice junctions |
Genomics |
High |
7507076
|
| 1993 |
VCAM-1 is constitutively expressed on murine microvascular endothelium and is strongly upregulated by TNF, IL-1, or LPS (but not PMA or staurosporine). Antibody blocking of VCAM-1 on endothelium or VLA-4 on leukocytes demonstrated that VCAM-1/VLA-4 interaction mediates the adhesion of splenocytes, thymocytes, P815 mastocytoma cells, mast/basophil cells, Molt-4 cells, and eosinophils to cytokine-activated microvascular endothelium. |
Flow cytometry, monoclonal antibody blocking adhesion assay, rosette technique |
Cellular immunology |
Medium |
7680963
|
| 1995 |
VCAM-1/CD106 expressed on TCR-γδ T cell clones undergoes regulated proteolytic shedding by a zinc-activated metalloprotease to generate a soluble 100-kDa form. Phorbol ester increases soluble CD106 release and reduces membrane-bound form; EDTA and 1,10-phenanthroline (metalloprotease inhibitors) specifically block this conversion. |
Immunoprecipitation, SDS-PAGE, phorbol ester stimulation, metalloprotease inhibitor experiments |
Journal of immunology |
Medium |
7529789
|
| 1995 |
Both domain 1 and domain 4 of the 7-domain form of VCAM-1 can independently support VLA-4 (α4β1)-mediated monocyte transendothelial migration; antibodies to each domain alone only partially block migration, but their combination fully blocks CD18-independent, VLA-4-mediated migration across CHO-VCAM-1 transfectants and IL-1-activated endothelium. |
Domain-specific monoclonal antibody blocking, CHO cell transfection, transendothelial migration assay under chemotactic gradient |
Journal of immunology |
Medium |
7545712
|
| 1997 |
Cross-linking of VCAM-1 on endothelial cells (ECV304) or its counter-receptor VLA-4 on Jurkat T cells activates the phosphoinositide pathway (IP3 production) and triggers a biphasic intracellular Ca2+ mobilization. Cell-cell contact via VLA-4/VCAM-1 interaction induces mutual Ca2+ signaling in both cell types, blocked ~80% by non-cross-linked anti-VLA-4 or anti-VCAM-1 antibodies. |
Fura-2 fluorimetry, confocal microscopy, IP3 assay, antibody blocking, co-culture experiments |
European journal of immunology |
Medium |
9209507
|
| 1997 |
p38 MAP kinase signaling regulates VCAM-1 surface expression at a post-transcriptional level in TNFα-stimulated endothelial cells. The specific p38 inhibitor SB203580 suppressed TNFα-induced VCAM-1 surface expression without affecting VCAM-1 mRNA accumulation, and also blocked MAPKAP kinase-2 activation and Hsp27 phosphorylation. In contrast, ICAM-1 surface expression was unaffected by p38 inhibition. |
Kinase activity assay (MAPKAP-K2), phosphorylation assay (Hsp27), flow cytometry for surface expression, Northern blot for mRNA, pharmacological inhibitor (SB203580) |
Biochemical and biophysical research communications |
Medium |
9020057
|
| 1998 |
Thrombin induces VCAM-1 and ICAM-1 expression on HUVECs via its specific receptor (thrombin receptor-activating peptide mimics the effect; hirudin inhibits it), independent of IL-1 or TNFα signaling. Thrombin-induced VCAM-1 and ICAM-1 were functionally active, supporting monocyte/PBMC adhesion that was blocked by anti-CD18 and anti-CD49d antibodies. |
ELISA, RT-PCR, flow cytometry, thrombin receptor-activating peptide, antibody blocking, monocyte adhesion assay |
Blood |
Medium |
9694714
|
| 1998 |
IRF-1 (interferon regulatory factor 1) is required for IFN-α and IFN-γ enhancement of TNF-induced VCAM-1 transcription in endothelial cells. IFN treatment increased nuclear IRF-1 levels and IRF-1 binding to the VCAM-1 promoter; transfection of an IRF-1 construct substituted for IFN; and transfection with IRF-2 (a competitive IRF-1 inhibitor) reduced TNF-induced VCAM-1 expression. The primary NF-κB-driven pathway was not affected. |
CAT reporter gene assay, EMSA (IRF-1 binding to promoter), Western blot (nuclear IRF-1), transfection of IRF-1 and IRF-2 constructs |
The Journal of experimental medicine |
High |
9625761
|
| 2000 |
VCAM-1 (CD106) expressed on rheumatoid arthritis synovial fibroblasts (FLS) mediates B cell survival and Bcl-xL upregulation in a contact-dependent manner. Blocking anti-CD106 (but not anti-CD54/ICAM-1) antibodies abolished FLS-induced B cell protection from apoptosis and Bcl-xL induction; cross-linking CD49d/CD29 (VLA-4) on B cells recapitulated the survival signal. |
Apoptosis assay (trypan blue, annexin V, propidium iodide, Hoechst), Western blot (Bcl-xL), antibody blocking, VLA-4 cross-linking |
Journal of immunology |
Medium |
10623863
|
| 2001 |
During G-CSF-induced hematopoietic progenitor cell (HPC) mobilization, neutrophil-derived serine proteases (neutrophil elastase and cathepsin G) cleave VCAM-1 expressed on bone marrow stromal cells, reducing VCAM-1 levels in vivo and thereby contributing to HPC release from the bone marrow niche. |
In vivo murine mobilization model, VCAM-1 protein quantification in bone marrow, protease activity assays, identification of neutrophil elastase and cathepsin G as VCAM-1 cleavage enzymes |
Blood |
Medium |
11520773
|
| 2001 |
VCAM-1 plays a dominant role in the initiation of atherosclerosis. Mice with a hypomorphic Vcam1(D4D) allele (2–8% of wild-type VCAM-1 levels) crossed into an LDL-receptor-null background showed significantly reduced early atherosclerotic lesion area compared with wild-type littermates on a cholesterol-enriched diet, while ICAM-1 deficiency alone or combined with VCAM-1 deficiency did not alter nascent lesion formation. |
In vivo murine genetic model (hypomorphic Vcam1 allele), en face oil red O aortic staining, lipid and leukocyte profiling |
The Journal of clinical investigation |
High |
11375415
|
| 2001 |
Fibroblast-like synoviocytes (FLS) support B-cell pseudoemperipolesis via co-dependent expression of SDF-1 (chemokine) and CD106 (VCAM-1). SDF-1/CXCR4 signaling was required for B cell chemotaxis beneath FLS, while CD106 engagement of VLA-4 (α4β1/CD49d) was required for firm adhesion/migration; antibodies to CD49d, CD106, or the CS-1 fibronectin peptide inhibited pseudoemperipolesis. Dermal fibroblasts (which express SDF-1 but not CD106) required IL-4-induced CD106 upregulation to support the process. |
Antibody blocking assay, pertussis toxin inhibition, cytokine stimulation (IL-4), co-culture migration assay |
The Journal of clinical investigation |
Medium |
11160154
|
| 2002 |
VCAM-1 signals through endothelial cells during lymphocyte migration via NADPH oxidase-generated reactive oxygen species (ROS), which subsequently activate matrix metalloproteinases. These signals are required for endothelial cell shape changes that open an 'endothelial cell gate' for leukocyte transmigration, after which endothelial contacts are re-established. |
Review synthesizing experimental evidence: NADPH oxidase inhibition, ROS measurement, MMP activation assay, migration assay |
Molecular immunology |
Low |
12431382
|
| 2006 |
Eosinophil adhesion to the module 1–3 region (6d-VCAM-1) is mediated exclusively by α4β1 (CD49d/CD29), whereas adhesion to the module 4–7 region is mediated by both α4β1 and αMβ2 (CD11b/CD18). αMβ2 engagement of module 4 is PI3K-dependent and modulates α4β1-mediated adhesion under flow conditions. |
Domain-specific recombinant VCAM-1 constructs, antibody blocking, PI3K inhibitor, leukemic cell lines lacking αMβ2, static and flow adhesion assays |
The Journal of biological chemistry |
High |
16943205
|
| 2008 |
Canonical Wnt/β-catenin signaling negatively regulates VCAM-1 expression on two types of bone marrow cells (stromal and hematopoietic). Wnt3a-mediated VCAM-1 downregulation was blocked by intracellular (Axin) or extracellular (Dkk-1) Wnt inhibitors. LPS restored VCAM-1 expression in Wnt3a-treated cells, indicating functional cross-talk between Wnt and TLR4 pathways. |
Recombinant Wnt ligands, retroviral Wnt transduction, Wnt-secreting co-culture, flow cytometry, Axin and Dkk-1 pathway inhibitors, in vivo transplantation |
Experimental hematology |
Medium |
18951693
|
| 2012 |
Nuclear-localized FAK regulates VCAM-1 expression via two mechanisms: (1) kinase-active FAK facilitates TNFα-induced MAPK signaling and maintains GATA4, a transcription factor required for VCAM-1 production; (2) kinase-inhibited FAK translocates to the nucleus where its FERM domain directly binds GATA4 and promotes CHIP E3 ligase-dependent GATA4 polyubiquitination and degradation, thereby suppressing VCAM-1 expression. FAK inhibition prevented TNFα-induced VCAM-1 expression in endothelial cells in vivo and during development. |
FAK pharmacological inhibition, genetic FAK knockout, nuclear fractionation, direct binding assay (FAK-FERM to GATA4), ubiquitination assay, in vivo heart vessel-associated endothelial cell experiments |
The Journal of cell biology |
High |
22734001
|
| 2012 |
IRF-1 and miR-126 reciprocally regulate VCAM-1 expression in endothelial cells in response to triglyceride-rich lipoproteins (TGRL). Proatherogenic TGRL increases IRF-1 expression/activity and decreases miR-126, enhancing VCAM-1; antiatherogenic TGRL does the opposite. Overexpression or silencing of IRF-1 or miR-126 recapitulates proatherogenic or antiatherogenic VCAM-1 regulation. |
Gene overexpression and siRNA knockdown, IRF-1 activity assay, miR-126 expression analysis, VCAM-1 protein/mRNA assay, monocyte adhesion assay |
Circulation research |
Medium |
22874466
|
| 2015 |
Tumor-derived SPARC induces vascular permeability and cancer cell extravasation through endothelial VCAM1 and downstream p38 MAPK signaling. SPARC deficiency abolished tumor-initiated lung capillary permeability and prevented extravasation; SPARC overexpression enhanced them. Blocking VCAM1 specifically impeded SPARC-induced endothelial permeability and melanoma extravasation. |
SPARC knockout/overexpression, anti-VCAM1 blocking antibody, in vivo lung permeability assay, extravasation/metastasis assay, p38 MAPK inhibition, comparative secretome proteomics |
Nature communications |
High |
25925867
|
| 2015 |
VCAM-1+ red pulp macrophages in the spleen retain hematopoietic stem cells (HSCs) via VCAM-1-mediated adhesion. Nanoparticle-RNAi silencing of M-CSFR blocked splenic macrophage maturation and reduced VCAM-1 expression; depletion of macrophages (CD169-iDTR mice) or specific VCAM-1 silencing in macrophages released HSCs from spleen and reduced leukocytosis/inflammation in myocardial infarction and atherosclerosis models. |
Nanoparticle-mediated in vivo RNAi, CD169-iDTR macrophage depletion, flow cytometry, murine MI and atherosclerosis models |
The Journal of experimental medicine |
High |
25800955
|
| 2016 |
oxLDL-induced VCAM-1 expression and monocyte adhesion in endothelial cells requires FAK-dependent activation of p90 RSK, which in turn activates IKKβ and NF-κB. Inhibiting RSK blocks all downstream NF-κB and VCAM-1 induction. Endothelial-specific kinase-dead FAK transgenic mice show reduced RSK activity, decreased VCAM-1 expression, and reduced macrophage accumulation in early atherosclerosis. |
RSK pharmacological inhibition, FAK kinase-dead transgenic mice, NF-κB/IKKβ activity assay, VCAM-1 protein/mRNA, monocyte adhesion assay, in vivo atherosclerosis model |
Journal of cell science |
High |
26906414
|
| 2017 |
VCAM-1 expressed on radial glial cells (RGCs) during embryonic development is required for the embryonic origin of adult neural stem cells (NSCs). Loss of VCAM1 in embryonic RGCs stimulates premature neuronal differentiation, prevents quiescence of slowly-dividing RGCs, and diminishes postnatal/adult NSC numbers and V-SVZ regeneration. Mechanistically, VCAM1 signals through its intracellular domain to regulate β-catenin signaling in a context-dependent manner. |
Conditional Vcam1 knockout mice, lineage tracing, BrdU/EdU pulse-chase, adult NSC quantification, V-SVZ regeneration assay, β-catenin reporter assay |
Neuron |
High |
28728023
|
| 2017 |
VCAM-1 synergizes with Notch ligand DLL4 to enhance Notch signaling and progenitor T-cell differentiation from HSPCs in vitro. VCAM-1 additionally promotes an inflammatory transcriptional program in nascent HSPCs. Combined DLL4+VCAM-1 presentation on an engineered surface enhanced downstream progenitor T-cell output ~80-fold compared to DLL4 alone. |
Engineered stromal cell-free niche with defined protein presentation, flow cytometry for T-cell differentiation markers, Notch signaling reporter, transcriptional profiling |
Nature methods |
Medium |
28394335
|
| 2018 |
VCAM-1+ macrophage-like 'usher cells' in the zebrafish caudal haematopoietic tissue (CHT) patrol the inner surface of the venous plexus and interact with HSPCs via ITGA4 (integrin α4)-dependent interactions to direct HSPC retention in homing hotspots. |
High-resolution live imaging in zebrafish, cell-labelling system, ITGA4 blocking/genetic experiments, VCAM-1 expression characterization |
Nature |
High |
30455424
|
| 2019 |
Brain endothelial VCAM1 mediates the detrimental effects of aged plasma on young brains. Aged mouse hippocampal BECs upregulate VCAM1; plasma from aged humans/mice increases VCAM1 in cultured BECs and young mouse hippocampi. Systemic anti-VCAM1 antibody or genetic Vcam1 ablation in BECs reverses microglial reactivity and cognitive deficits in aged mice and counteracts effects of aged plasma in young mice. |
Parabiosis/plasma transfer model, conditional BEC-specific Vcam1 knockout mice, anti-VCAM1 antibody treatment, cognitive testing, microglial activation assays |
Nature medicine |
High |
31086348
|
| 2019 |
Phc2, an epigenetic regulator, controls HSPC mobilization from bone marrow by transcriptionally repressing Vcam1 in bone marrow stromal cells via H3K27me3 and H2AK119ub histone modifications. Phc2 genetic ablation causes de-repression of Vcam1, retention of HSPCs, and systemic immunodeficiency; pharmacological inhibition of VCAM-1 in Phc2-deficient mice reverses these symptoms. |
Phc2 knockout mice, HSPC mobilization assay, chromatin immunoprecipitation (H3K27me3, H2AK119ub), VCAM-1 pharmacological inhibition rescue experiment |
Nature communications |
High |
31375680
|
| 2020 |
TRIM65, an E3 ubiquitin ligase, directly interacts with VCAM-1 protein and promotes its polyubiquitination and proteasomal degradation, limiting the duration and magnitude of VCAM-1-mediated inflammation. TRIM65 and VCAM-1 expression are inversely correlated during TNFα-induced endothelial activation; wild-type but not E3-ligase-dead TRIM65 promotes VCAM-1 ubiquitination; TRIM65 knockdown attenuates VCAM-1 degradation. TRIM65-deficient mice show enhanced LPS-induced pulmonary inflammation. |
Co-immunoprecipitation, ubiquitination assay, E3-ligase-dead mutant, siRNA knockdown, TRIM65 KO mice, LPS-induced pulmonary inflammation model |
Journal of molecular cell biology |
High |
31310649
|
| 2021 |
HDAC1/2 promote VCAM-1 expression by suppressing STAT3 acetylation-dependent DNMT1 recruitment to the GATA6 promoter, thereby preventing hypermethylation of GATA6 CpG regions. HDAC1/2 inhibition (Romidepsin) enhanced STAT3 acetylation, increased DNMT1-STAT3 interaction, hypermethylated the GATA6 promoter, reduced GATA6 and VCAM-1 expression, and decreased monocyte adhesion. Blocking STAT3 acetylation (Lys685Arg mutation) disrupted DNMT1-STAT3 interaction and reversed these effects. |
Romidepsin treatment, siRNA knockdown of HDAC1/2, methylation-specific PCR, ChIP (STAT3 binding to GATA6 promoter), STAT3 Lys685Arg point mutation, Apoe-/- mouse atherosclerosis model |
Theranostics |
High |
33859766
|
| 2021 |
Macrophage VLA4 (CD49d)-endothelial VCAM1 interaction promotes vascular permeability in ovarian cancer ascites. Mechanistically, VCAM1 engagement activates RAC1 and ROS, leading to phosphorylation of PYK2 and VE-cadherin, thereby increasing endothelial paracellular permeability. Downregulation of VLA4 on M2 macrophages reduces RAC1/ROS/p-PYK2/p-VE-cad signaling and enhances barrier function. Targeting VLA4/VCAM1 augmented vascular integrity and abrogated ascites formation in vivo. |
VLA4/VCAM1 overexpression and knockdown, RAC1 and ROS assays, p-PYK2/p-VE-cadherin Western blot, in vivo permeability assay, anti-VLA4 antibody treatment, bevacizumab combination |
The Journal of clinical investigation |
High |
33295887
|
| 2021 |
Membrane-bound SCF (mSCF) and VCAM-1 synergistically regulate HSC morphology and adhesion via PI3K signaling and cytoskeletal reorganization. HSCs cluster mSCF at the HSC-substrate interface and form a polarized morphology with a large protrusion when both mSCF and VCAM-1 are present on a supported lipid bilayer. This synergy dramatically enhances HSC adhesion and promotes nuclear retention of FOXO3a, a key HSC maintenance factor, reducing its loss induced by soluble SCF. |
Supported lipid bilayer (SLB) system, live cell imaging, PI3K pharmacological inhibition, cytoskeletal inhibitors, FOXO3a nuclear localization assay |
The Journal of cell biology |
High |
34402812
|
| 2022 |
VCAM1 on hematopoietic stem cells (HSCs) and leukaemic stem cells (LSCs) functions as a 'don't-eat-me' signal in the context of MHC-I presentation, protecting them from phagocyte-mediated clearance. Mechanistically, VCAM1 'don't-eat-me' activity requires β2-microglobulin-dependent MHC-I presentation on HSCs and paired Ig-like receptor-B (PIR-B) on phagocytes. Vcam1 deletion in the setting of haplotype mismatch leads to HSC clearance by mononuclear phagocytes and impaired haematopoietic recovery. In AML, VCAM1 inhibition or deletion reduces leukaemia burden and extends survival. |
Vcam1 conditional knockout, haplotype-mismatched transplantation, MHC-I (β2m) genetic manipulation, PIR-B-expressing phagocyte assays, AML mouse model (VCAM1 inhibition) |
Nature cell biology |
High |
35210567
|
| 2022 |
VCAM-1 and DLL4 synergize to activate Notch signaling in nascent HSPCs and enhance T-cell-competent progenitor output ~80-fold from human PSCs; VCAM1 additionally promotes an inflammatory transcriptional program during the endothelial-to-haematopoietic transition. |
Defined serum- and feeder-free PSC differentiation system with DLL4 and VCAM1 proteins, Notch signaling reporter, transcriptional profiling, in vivo thymus colonization assay |
Science advances |
Medium |
36001668
|
| 2023 |
IL-33-induced VCAM1 in microglia directs microglial chemotaxis toward amyloid-beta (Aβ) plaques by sensing plaque-associated ApoE. Disrupting the VCAM1-ApoE interaction abolishes microglial Aβ chemotaxis and decreases Aβ clearance. Higher CSF soluble VCAM1 in AD patients correlates with impaired microglial Aβ chemotaxis. |
IL-33 stimulation, VCAM1 gain/loss of function in microglia, functional screening for chemotaxis, VCAM1-ApoE interaction blocking, in vivo Aβ clearance assay, human CSF correlation |
Nature aging |
High |
37735240
|
| 2023 |
VCAM-1+ endothelial cell-derived extracellular vesicles (EVs) mediate rapid neutrophil mobilization from the spleen to peripheral blood after myocardial infarction. CRISPR/Cas9-mediated deletion of VCAM-1 from endothelial cells removed the ability of EC-EVs to mobilize splenic neutrophils. VCAM-1+ EVs accumulate in the spleen and induce local inflammatory gene/chemokine expression. |
CRISPR/Cas9 VCAM-1 KO in parent endothelial cells, EV isolation/characterization, in vivo EV administration, splenic neutrophil mobilization assay, gene expression profiling |
Cardiovascular research |
High |
35134856
|
| 2024 |
In the AKI-to-CKD transition, proinflammatory cytokines (TNF-α and IL-1β) induce VCAM-1 expression in proximal tubule cells via NF-κB signaling (requiring MyD88/TRIF adaptors). TNF-α stimulation or VCAM-1 overexpression increases CD45+ splenocyte adhesion to tubular monolayers; NF-κB inhibition or Vcam1 genetic deletion suppresses TNF-α-induced splenocyte adhesion, demonstrating a proximal tubule-immune cell cross-talk role for VCAM-1. |
TNF-α/IL-1β stimulation of primary renal cells, NF-κB pharmacological inhibition, MyD88/TRIF genetic deletion, VCAM-1 overexpression, splenocyte adhesion assay, single-cell transcriptomics of patient biopsies |
American journal of physiology. Renal physiology |
Medium |
39116349
|
| 2015 |
VCAM-1 and VAP-1 on tumor-activated pulmonary endothelium recruit myeloid cells that promote tumor cell survival and metastasis. VCAM-1 induction depends on tumor cell-clot formation (blocked by tissue factor pathway inhibitor or hirudin). Anti-VCAM-1 blocking antibody reduces myeloid cell recruitment and tumor cell survival without affecting tumor cell adhesion. |
VCAM-1 antibody blocking, tissue factor pathway inhibitor, hirudin treatment, in vivo myeloid cell recruitment assay, tumor survival/metastasis assay |
Blood |
Medium |
23407548
|
| 2020 |
CAF-derived VCAM1 (upregulated by H. pylori infection via JAK/STAT1 signaling) molecularly interacts with integrin αvβ1/5 on gastric cancer cells to facilitate tumor invasion. The kinetic binding interaction between VCAM1 and integrin αvβ1/5 was directly measured by biolayer interferometry. |
RNA-seq, biolayer interferometry (direct binding kinetics), spheroid invasion assay, zebrafish xenograft model, JAK/STAT1 inhibition |
Oncogene |
Medium |
32034307
|
| 2015 |
Endothelial Notch1 intracellular domain (N1ICD) upregulates VCAM1 expression and amplifies IL-1β-mediated VCAM1 induction through a Notch1-Jagged1 autocrine circuit. Forced N1ICD expression upregulated VCAM1 per se; γ-secretase inhibition or Notch1/Jagged1 silencing reduced IL-1β-mediated VCAM1 induction. IL-1β decreases Notch1 mRNA but maintains active N1ICD protein levels. |
γ-secretase inhibitor, Notch1/Jagged1 siRNA silencing, N1ICD forced expression, Western blot (Notch1ICD, Jagged1), VCAM1 promoter reporter, liver inflammation model |
Oncotarget |
Medium |
26646450
|
| 2017 |
FSH promotes endothelial VCAM-1 expression via FSHR located in membrane caveolae interacting with caveolin-1 and GαS, leading to cAMP/PKA elevation and PI3K/Akt/mTOR/NF-κB activation. Disruption of caveolae or caveolin-1 silencing blocks FSH-induced signaling and VCAM-1 expression. FSH increases monocyte adhesion to HUVECs, reversed by VCAM-1 neutralizing antibody. |
Luciferase reporter assay, transfection, flow chamber adhesion assay, Western blot, caveolae disruption, caveolin-1 siRNA, PI3K/Akt/mTOR inhibitors, NF-κB luciferase, VCAM-1 neutralizing antibody, ApoE KO atherosclerosis mouse model |
Theranostics |
Medium |
29187895
|
| 2022 |
In MLL-fusion AML, IMPDH inhibition induces overactivation of TLR-TRAF6-NF-κB signaling and upregulation of VCAM1, which contributes to the antileukemia effect. Combined treatment with IMPDH inhibitors and TLR1/2 agonist effectively inhibited MLL-fusion AML development in vivo. |
In vitro IMPDH inhibitor treatment, NF-κB signaling assay, VCAM1 expression analysis, in vivo AML mouse model, TLR1/2 agonist combination |
EMBO molecular medicine |
Medium |
36453131
|
| 2019 |
VCAM1 expression in ovarian theca and stromal cells is induced by androgen receptor (AR) signaling; AR antagonist flutamide markedly reduces VCAM1 mRNA and protein in PCOS-derived theca cells. VCAM1 expression is specifically elevated in NR2F2/COUPTF-II lineage theca cells, not granulosa cells, of DHT-treated mice. LH (equine chorionic gonadotropin) transiently induces VCAM1, while hCG (superovulatory dose) potently suppresses it. |
Genome-wide microarray, DHT-treatment mouse model, AR antagonist (flutamide) treatment, immunohistochemistry, RT-PCR, PCOS-derived human theca cell culture |
Endocrinology |
Medium |
30951142
|
| 2014 |
VCAM1 on the uterine endometrial epithelium and trophoblast ITGA4 (integrin α4) mediate bovine conceptus adhesion to the uterine endometrium during implantation. VCAM1 and ITGA4 expression are mutually upregulated by co-culture of endometrial epithelial cells (EECs) with bovine trophoblast CT1 cells and by uterine flushings. ITGA4 protein is localized specifically to trophoblasts in day-22 pregnant uteri. |
Co-culture of EEC and CT1 trophoblast cells, immunohistochemistry (VCAM1, ITGA4 localization), RT-PCR, Western blot, uterine flushing treatment |
Reproduction (Cambridge, England) |
Medium |
24803492
|
| 2022 |
In AML driven by IRF7 loss, VCAM1 is upregulated (correlated with elevated LSC levels), and VCAM1-VLA-4 axis mediates intracerebral invasion of AML cells. Blocking the VCAM1-VLA-4 axis delayed disease progression and attenuated intracerebral invasion in IRF7-/- AML mouse models. |
IRF7 KO and overexpression in MLL-AF9 AML model, xenograft mouse model, VCAM1 expression analysis, anti-VCAM1/anti-VLA-4 antibody blocking, intracranial invasion assay |
Oncogene |
Medium |
35256780
|
| 2022 |
Notch1-c-myc-VCAM1 signaling axis drives macrophage-dependent HCC transendothelial migration and pulmonary metastasis. Elevated Notch1 increases c-myc, which transcriptionally upregulates VCAM1. Silencing c-myc prohibits tumorigenicity; VCAM1 depletion reduces spontaneous lung metastasis without affecting primary tumor growth. Macrophage depletion or blockade of macrophage α4β1-integrin (VCAM1 receptor) reduces lung nodule formation. |
N1ICD overexpression in LPC, c-myc and VCAM1 siRNA/shRNA, orthotopic rat liver tumor model, macrophage depletion, α4β1 integrin blocking antibody, experimental metastasis model |
Oncogene |
Medium |
35256782
|
| 2021 |
NF-κB regulates CD106 (VCAM1) expression in bone marrow mesenchymal stem cells, and CD106 supports hematopoiesis. CD106+ MSCs show increased in vitro capillary tube-like formation, vasculogenesis, and in vivo engraftment of CD34+ cells compared to CD106- MSCs. TNF-α and LPS stimulation of MSCs confirms NF-κB-mediated induction of VCAM1. |
Flow cytometry, Illumina HiSeq sequencing, qRT-PCR, Western blot, NF-κB inhibition (blockade assay, immunofluorescence), CD34+ cell engraftment in NOD/SCID mice, colony-forming assays |
Stem cell research & therapy |
Medium |
28764810
|