ICAM-5—A novel two-facetted adhesion molecule in the mammalian brain

Gahmberg, Carl G.; Tian, Li; Lin, Ning; Nyman-Huttunen, Henrietta

doi:10.1016/j.imlet.2008.02.004

Cited by 47 publications

(41 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, a plausible role for ICAM4 and ICAM5 in SLE pathogenesis is less clear because they are preferentially expressed in red blood cells and brain, respectively 13 14…”

Section: Discussionmentioning

confidence: 99%

Variation in the ICAM1–ICAM4–ICAM5 locus is associated with systemic lupus erythematosus susceptibility in multiple ancestries

et al. 2012

View full text Add to dashboard Cite

Objective Systemic lupus erythematosus (SLE; OMIM 152700) is a chronic autoimmune disease for which the aetiology includes genetic and environmental factors. ITGAM, integrin αΜ (complement component 3 receptor 3 subunit) encoding a ligand for intracellular adhesion molecule (ICAM) proteins, is an established SLE susceptibility locus. This study aimed to evaluate the independent and joint effects of genetic variations in the genes that encode ITGAM and ICAM. Methods The authors examined several markers in the ICAM1–ICAM4–ICAM5 locus on chromosome 19p13 and the single ITGAM polymorphism (rs1143679) using a large-scale case–control study of 17 481 unrelated participants from four ancestry populations. The single marker association and gene–gene interaction were analysed for each ancestry, and a meta-analysis across the four ancestries was performed. Results The A-allele of ICAM1–ICAM4–ICAM5 rs3093030, associated with elevated plasma levels of soluble ICAM1, and the A-allele of ITGAM rs1143679 showed the strongest association with increased SLE susceptibility in each of the ancestry populations and the trans-ancestry meta-analysis (ORmeta=1.16, 95% CI 1.11 to 1.22; p=4.88×10−10 and ORmeta=1.67, 95% CI 1.55 to 1.79; p=3.32×10−46, respectively). The effect of the ICAM single-nucleotide polymorphisms (SNPs) was independent of the effect of the ITGAM SNP rs1143679, and carriers of both ICAM rs3093030-AA and ITGAM rs1143679-AA had an OR of 4.08 compared with those with no risk allele in either SNP (95% CI 2.09 to 7.98; p=3.91×10−5). Conclusion These findings are the first to suggest that an ICAM–integrin-mediated pathway contributes to susceptibility to SLE.

show abstract

“…However, a plausible role for ICAM4 and ICAM5 in SLE pathogenesis is less clear because they are preferentially expressed in red blood cells and brain, respectively 13 14…”

Section: Discussionmentioning

confidence: 99%

Variation in the ICAM1–ICAM4–ICAM5 locus is associated with systemic lupus erythematosus susceptibility in multiple ancestries

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Neuronmicroglial inhibitory interactions are facilitated by binding of a variety of neuronal immunomodulators to their cognate receptors expressed predominantly on microglia, such as CD200/CD200R (85,86), CX3CL1 (fractalkine)/CX3CLR1 (87, 88), CD22/CD45 (89), CD172A/CD47 (90), CD95/APO-1, and ICAM5/lymphocyte function-associated antigen-1 (LFA1) (91). Dysregulated neuronmicroglia communication has been implicated in neurodegenerative diseases (92).…”

Section: Loss Of Inhibitory Signalsmentioning

confidence: 99%

Microglia in Alzheimer’s disease

Sarlus

Heneka

2017

Journal of Clinical Investigation

671

561

View full text Add to dashboard Cite

“…The ICAM family consists of five subfamilies (ICAM-1 to ICAM-5) of heavily glycosylated cell surface receptors with common functional or structural homologies (9)(10)(11)(12). These proteins contain extracellular domains, transmembrane residues and cytoplasmic tail residues.…”

Section: Introductionmentioning

confidence: 99%

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

Park

et al. 2009

Int J Oncol

View full text Add to dashboard Cite

Abstract.We have previously reported that intercellular adhesion molecule-3 (ICAM-3) is associated with an increase of cellular radio-resistance and cancer cell proliferation. In this study, we hypothesized that ICAM-3 has an additional effect on cancer cell migration and invasion because molecules induced by ICAM-3 are known as regulators of cell migration and invasion. To examine this hypothesis, we used NCI-H1299 non-small cell lung cancer (NSCLC) cell line (p53 and PTEN null cell) and constructed an ICAM-3-over-expressing stable transfectant, which exhibited increased cell migration and invasion. The increased migration and invasion resulted from up-regulation of expression and activities of MMP-2 and MMP-9. ICAM-3 also increased Akt phosphorylation, which caused an increase in cellular migration/invasion and MMP activities. Activity of several transcriptional factors located downstream in the Akt pathway was also tested, and constitutive activation of adenosine 3', 5'-monophosphate response element-binding protein (CREB) by ICAM-3 was detected. Blockage of the Akt pathway attenuated CREB activation, and a decrease in CREB expression reduced cellular migration/invasion and activity of MMPs. This result indicates that CREB functions in the signaling pathway between Akt and MMP. We also showed ICAM-3-induced cell migration and invasion in NCI-H460 NSCLC cells (wild-type p53 and PTEN cell) through the same signaling pathway. Taken together, our findings suggest that ICAM-3 stimulates cancer cell migration/ invasion via ICAM-3/Akt/CREB/MMP pathway regardless of p53 and PTEN status, and this reflects the possibility that ICAM-3 could be considered as a candidate for anti-cancer drug development and as a cancer diagnostic marker.

show abstract

ICAM-5—A novel two-facetted adhesion molecule in the mammalian brain

Cited by 47 publications

References 70 publications

Variation in the ICAM1–ICAM4–ICAM5 locus is associated with systemic lupus erythematosus susceptibility in multiple ancestries

Variation in the ICAM1–ICAM4–ICAM5 locus is associated with systemic lupus erythematosus susceptibility in multiple ancestries

Microglia in Alzheimer’s disease

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

Contact Info

Product

Resources

About