Annexin A2 Limits Neutrophil Transendothelial Migration by Organizing the Spatial Distribution of ICAM-1

Heemskerk, Niels; Asimuddin, Mohammed; Oort, Chantal; Rijssel, Jos van; Buul, Jaap D. van

doi:10.4049/jimmunol.1501322

Cited by 13 publications

(7 citation statements)

References 53 publications

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“…Down-regulation of VE-PTP or its dissociation from VEC is followed by leukocyte transmigration across inflamed endothelium ( Nottebaum et al, 2008 ; Vockel and Vestweber, 2013 ), providing a possible explanation for our observation of increased numbers of neutrophils in the posthypoxic Anxa2 −/− lung parenchyma. Maldistribution of intercellular adhesion molecule 1 has been found to occur on the surface of TNFα-treated, ANXA2-depleted ECs and can contribute to augmented neutrophil transmigration ( Heemskerk et al, 2016 ). This phenomenon could be relevant in the hypoxic Anxa2 −/− mouse, even though baseline expression of cell surface intercellular adhesion molecule and pY14-caveolin did not differ between the two genotypes.…”

Section: Resultsmentioning

confidence: 99%

Annexin A2 supports pulmonary microvascular integrity by linking vascular endothelial cadherin and protein tyrosine phosphatases

Luo

Flood

Almeida

et al. 2017

Journal of Experimental Medicine

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Section: Resultsmentioning

confidence: 99%

Annexin A2 supports pulmonary microvascular integrity by linking vascular endothelial cadherin and protein tyrosine phosphatases

Luo

Flood

Almeida

et al. 2017

Journal of Experimental Medicine

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“…ADAM10 cellular localization is regulated by tetraspanins [34], which form specialized microdomains within the cell membrane (tetraspanin-enriched membrane rafts). Interestingly, upon clustering/leukocyte binding, ICAM-1 has been reported to be recruited to tetraspanin microdomains [35,36] as well as caveolin-rich lipid rafts [37]. It remains to be determined if the ADAM10-ICAM-1 interaction depends on and is regulated by the presence of such membrane raft localization.…”

Section: Discussionmentioning

confidence: 99%

ADAM10-Mediated Cleavage of ICAM-1 Is Involved in Neutrophil Transendothelial Migration

Morsing

Rademakers

Brouns

et al. 2021

Cells

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To efficiently cross the endothelial barrier during inflammation, neutrophils first firmly adhere to the endothelial surface using the endothelial adhesion molecule ICAM-1. Upon actual transmigration, the release from ICAM-1 is required. While Integrin LFA1/Mac1 de-activation is one described mechanism that leads to this, direct cleavage of ICAM-1 from the endothelium represents a second option. We found that a disintegrin and metalloprotease 10 (ADAM10) cleaves the extracellular domain of ICAM-1 from the endothelial surface. Silencing or inhibiting endothelial ADAM10 impaired the efficiency of neutrophils to cross the endothelium, suggesting that neutrophils use endothelial ADAM10 to dissociate from ICAM-1. Indeed, when measuring transmigration kinetics, neutrophils took almost twice as much time to finish the diapedesis step when ADAM10 was silenced. Importantly, we found increased levels of ICAM-1 on the transmigrating neutrophils when crossing an endothelial monolayer where such increased levels were not detected when neutrophils crossed bare filters. Using ICAM-1-GFP-expressing endothelial cells, we show that ICAM-1 presence on the neutrophils can also occur by membrane transfer from the endothelium to the neutrophil. Based on these findings, we conclude that endothelial ADAM10 contributes in part to neutrophil transendothelial migration by cleaving ICAM-1, thereby supporting the release of neutrophils from the endothelium during the final diapedesis step.

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“…However, histamine does not invoke de novo synthesis of the adhesion molecules needed for leukocyte TEM. One of the most important of these is ICAM-1 (CD54) (8)(9)(10)(11), which can be upregulated by the membrane component of Gram-negative bacteria, LPS. Synthesis of endothelial (E)-selectin, another important adhesion molecule, is also induced (6,12,13).…”

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confidence: 99%

Double-Hit–Induced Leukocyte Extravasation Driven by Endothelial Adherens Junction Destabilization

Morsing

Al-Mardini

Stalborch

et al. 2020

The Journal of Immunology

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During inflammation, endothelial cells are bombarded with cytokines and other stimuli from surrounding cells. Leukocyte extravasation and vascular leakage are both prominent but believed to be uncoupled as they occur in separate spatiotemporal patterns. In this study, we investigated a "double-hit" approach on primary human endothelial cells primed with LPS followed by histamine. Using neutrophil transendothelial migration (TEM) under physiological flow assays, we found that an LPS-primed endothelium synergistically enhanced neutrophil TEM when additionally treated with histamine, whereas the effects on neutrophil TEM of the individual stimuli were moderate to undetectable. Interestingly, the double-hit-induced TEM increase was not due to decreased endothelial barrier, increased adhesion molecule expression, or Weibel-Palade body release. Instead, we found that it was directly correlated with junctional remodeling. Compounds that increased junctional "linearity" (i.e., stability) counteracted the double-hit effect on neutrophil TEM. We conclude that a compound, in this case histamine (which has a short primary effect on vascular permeability), can have severe secondary effects on neutrophil TEM in combination with an inflammatory stimulus. This effect is due to synergic modifications of the endothelial cytoskeleton and junctional remodeling. Therefore, we hypothesize that junctional linearity is a better and more predictive readout than endothelial resistance for compounds aiming to attenuate inflammation.

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Annexin A2 Limits Neutrophil Transendothelial Migration by Organizing the Spatial Distribution of ICAM-1

Cited by 13 publications

References 53 publications

Annexin A2 supports pulmonary microvascular integrity by linking vascular endothelial cadherin and protein tyrosine phosphatases

Annexin A2 supports pulmonary microvascular integrity by linking vascular endothelial cadherin and protein tyrosine phosphatases

ADAM10-Mediated Cleavage of ICAM-1 Is Involved in Neutrophil Transendothelial Migration

Double-Hit–Induced Leukocyte Extravasation Driven by Endothelial Adherens Junction Destabilization

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