ICAM-1/LFA-1 interaction contributes to the induction of endothelial cell-cell separation: implication for enhanced leukocyte diapedesis

Wee, Hyun; Oh, Hyun-Mee; Jo, Jae-Hyeok; Jun, Chang‐Duk

doi:10.3858/emm.2009.41.5.038

Cited by 32 publications

(27 citation statements)

References 26 publications

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“…Both methods have previously been observed in vitro and in vivo [7], [8], [9], [10], [11], [12], though it has been suggested that transmigration in vivo occurs predominantly through the endothelial cell-cell junctions in certain tissues [13]. Therefore, our first goal was to evaluate the frequency of paracellular versus transcellular transmigration in our system, since it is likely that the biophysical role of neutrophils may vary depending on the route taken.…”

Section: Resultsmentioning

confidence: 99%

“…Leukocytes readily exploit two different transmigration pathways in which they either squeeze through endothelial cell-cell junctions (paracellular route) or directly through ECs (transcellular route). In general, the preferential pathway taken depends in vitro on the type of ECs or in vivo by vascular location [7], [8], [9], [10], [11], [12], [13], and the biological signaling varies accordingly. For example, as a leukocyte migrates between EC borders, junctional proteins such as vascular endothelial cadherin (VE-cadherin) are laterally displaced to create an intercellular gap [10].…”

Section: Introductionmentioning

confidence: 99%

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Human Neutrophil Cytoskeletal Dynamics and Contractility Actively Contribute to Trans-Endothelial Migration

2013

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Transmigration through the endothelium is a key step in the immune response. In our recent work, the mechanical properties of the subendothelial matrix and biophysical state of the endothelium have been identified as key modulators of leukocyte trans-endothelial migration. Here, we demonstrated that neutrophil contractile forces and cytoskeletal dynamics also play an active biophysical role during transmigration through endothelial cell-cell junctions. Using our previously-established model for leukocyte transmigration, we first discovered that >93% of human neutrophils preferentially exploit the paracellular mode of transmigration in our in vitro model, and that is independent of subendothelial matrix stiffness. We demonstrated that inhibition of actin polymerization or depolymerization completely blocks transmigration, thus establishing a critical role for neutrophil actin dynamics in transmigration. Next, inhibition of neutrophil myosin II-mediated contractile forces renders 44% of neutrophils incapable of retracting their trailing edge under the endothelium for several minutes after the majority of the neutrophil transmigrates. Meanwhile, inhibition of neutrophil contractile forces or stabilization of microtubules doubles the time to complete transmigration for the first neutrophils to cross the endothelium. Notably, the time to complete transmigration is significantly reduced for subsequent neutrophils that cross through the same path as a previous neutrophil and is less dependent on neutrophil contractile forces and microtubule dynamics. These results suggest that the first neutrophil induces a gap in endothelial cell-cell adhesions, which “opens the door” in the endothelium and facilitates transmigration of subsequent neutrophils through the same hole. Collectively, this work demonstrates that neutrophils play an active biophysical role during the transmigration step of the immune response.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human Neutrophil Cytoskeletal Dynamics and Contractility Actively Contribute to Trans-Endothelial Migration

2013

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“…The K469E polymorphism is a non‐synonymous SNP located in the fifth immunoglobulin‐like domain of ICAM‐1, which is required for protein dimerization, surface presentation, and solubilization (Miller et al, ; Vora et al, ). It results in a change in glutamate (E) to lysine (K) in the immunoglobulin‐like domain 5 of the ICAM‐1 protein, which is critical for the activity of the ICAM‐1 protein to interact with LFA‐1 (Zhao et al, ; Wee et al, ). In addition, one study showed that this polymorphism affects ICAM‐1 mRNA splicing patterns and TPA‐induced apoptosis (Iwao, Morisaki, & Morisaki, ).…”

Section: Discussionmentioning

confidence: 99%

Association between K469E polymorphism of ICAM‐1 gene and susceptibility of ischemic stroke: An updated meta‐analysis

Nepal

Yadav

Kong

2019

Molec Gen & Gen Med

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Background The intercellular adhesion molecule‐1 (ICAM‐1)/leukocyte function associated antigen‐1 (LFA‐1) adhesion system regulates leukocyte interactions, migration, and adhesion, and appears to play an important role in atherosclerosis and thrombosis. Therefore, single nucleotide polymorphisms (SNPs) of the ICAM‐1 gene may strongly influence the expression and biological activity of ICAM‐1 and play a potentially important role in the pathogenesis of ischemic stroke. In the current meta‐analysis, we investigated the relationship between the ICAM‐1 gene K469E SNP and the risk of ischemic stroke. Methods Two investigators independently searched PubMed, Web of Science, Google Scholar, WANFANG, China National Knowledge Infrastructure (CNKI) and J‐STAGE for studies published from January 2000 to February 2019 without language restriction. The association of K469E polymorphism and ischemic stroke in three genetic models (allelic, recessive, and dominant) were evaluated using Pooled odds ratios (ORs) with 95% confidence intervals (CIs). Results Our study included 20 studies from four continents and four different countries, including 3,137 cases and 15,382 controls. Meta‐analysis results did not show a significant association between K469E polymorphism of ICAM‐1 gene and ischemic stroke when assuming allelic model (OR: 1.12; 95% CI: 0.8 to 1.55; p = 0.51; I 2 = 93%) or recessive model (OR: 1.28; 95% CI: 0.89 to 1.84; p = 0.18; I 2 = 82%) or dominant model (OR: 1.20; 95% CI: 0.92 to 1.56; p = 0.17; I 2 = 85%). However, in all three genetic models, subgroup analysis revealed that the K469E polymorphism of the ICAM‐1 gene is associated with ischemic stroke in the Caucasian population. Conclusion K469E polymorphism of ICAM‐1 gene might be a risk factor for ischemic stroke in Caucasians, which suggested that K469E polymorphism might help in early identification of those at risk and help in primary prevention of ischemic stroke.

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“…Initially, it was believed that tumor cell extravasation could be mechanistically similar to leukocyte extravasation, which occurs during an immune response. Indeed, cancer cells have been reported to migrate through the body of ECs via the "transcellular" route (57,73) and also between EC junctions via the "paracellular" route (145), two courses commonly used by leukocytes (2,17,18,121,130,144,148). During extravasation via the paracellular route, a leukocyte creates a small, localized gap in the vascular endothelial cadherin within the endothelium (121,130).…”

Section: Tumor Cell Extravasationmentioning

confidence: 98%

Physical Biology in Cancer. 4. Physical cues guide tumor cell adhesion and migration

Stroka

Κωνσταντόπουλος

2014

American Journal of Physiology-Cell Physiology

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As tumor cells metastasize from the primary tumor location to a distant secondary site, they encounter an array of biologically and physically heterogeneous microenvironments. While it is well established that biochemical signals guide all stages of the metastatic cascade, mounting evidence indicates that physical cues also direct tumor cell behavior, including adhesion and migration phenotypes. Physical cues acting on tumor cells in vivo include extracellular matrix mechanical properties, dimensionality, and topography, as well as interstitial flow, hydrodynamic shear stresses, and local forces due to neighboring cells. State-of-the-art technologies have recently enabled us and other researchers to engineer cell microenvironments that mimic specific physical properties of the cellular milieu. Through integration of these engineering strategies, along with physics, molecular biology, and imaging techniques, we have acquired new insights into tumor cell adhesion and migration mechanisms. In this review, we focus on the extravasation and invasion stages of the metastatic cascade. We first discuss the physical role of the endothelium during tumor cell extravasation and invasion and how contractility of endothelial and tumor cells contributes to the ability of tumor cells to exit the vasculature. Next, we examine how matrix dimensionality and stiffness coregulate tumor cell adhesion and migration beyond the vasculature. Finally, we summarize how tumor cells translate and respond to physical cues through mechanotransduction. Because of the critical role of tumor cell mechanotransduction at various stages of the metastatic cascade, targeting signaling pathways involved in tumor cell mechanosensing of physical stimuli may prove to be an effective therapeutic strategy for cancer patients.

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ICAM-1/LFA-1 interaction contributes to the induction of endothelial cell-cell separation: implication for enhanced leukocyte diapedesis

Cited by 32 publications

References 26 publications

Human Neutrophil Cytoskeletal Dynamics and Contractility Actively Contribute to Trans-Endothelial Migration

Human Neutrophil Cytoskeletal Dynamics and Contractility Actively Contribute to Trans-Endothelial Migration

Association between K469E polymorphism of ICAM‐1 gene and susceptibility of ischemic stroke: An updated meta‐analysis

Physical Biology in Cancer. 4. Physical cues guide tumor cell adhesion and migration

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