Cross-Linking of Brain Endothelial Intercellular Adhesion Molecule (ICAM)-1 Induces Association of ICAM-1 With Detergent-Insoluble Cytoskeletal Fraction

Amos, Claire; Romero, Ignacio A.; Schültze, Charlotte; Rousell, Jonathan; Pearson, Jeremy D.; Greenwood, John; Adamson, Peter

doi:10.1161/01.atv.21.5.810

Cited by 33 publications

(30 citation statements)

References 22 publications

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“…Cytoplasmic extensions of type I pneumocytes in human lung penetrate the basement membrane to contact the fibroblast (10). As observed in rabbits, human fibroblasts may also contact a capillary pericyte through an aperture in its basement membrane (9) or the endothelial cell in a similar fashion (11). In summary, 1, 3, 9, and 11 occur in rabbit, whereas 2 and 11 occur in human lung.…”

Section: B Preexisting Holes In the Basement Membranementioning

confidence: 74%

“…In a separate study, endothelial calcium increases were detected after antibody ligation of PECAM-1, even with Fab fragments, and the authors noted the effect was specific for certain antibodies (93). In vitro experiments with rat brain microvessel endothelial cells show cross-linking ICAM-1 results in Rho activation, phosphorylation of cytoskeletal proteins and transcription factors, and ICAM-1 association with the cytoskeleton (11,70). Similarly, in cultured human pulmonary microvascular endothelial cells treated with TNF-␣ for 24 h, ICAM-1-dependent neutrophil adhesion or ICAM-1 cross-linking induces cytoskeletal remodeling and phosphorylation and activation of p38 mitogen-activated protein kinase (MAPK).…”

Section: Neutrophil Migration Across Vascular Endotheliummentioning

confidence: 98%

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Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Burns

Smith²,

Walker³

2003

Physiological Reviews

266

273

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Neutrophil emigration in the lung differs substantially from that in systemic vascular beds where extravasation occurs primarily through postcapillary venules. Migration into the alveolus occurs directly from alveolar capillaries and appears to progress through a sequence of steps uniquely influenced by the cellular anatomy and organization of the alveolar wall. The cascade of adhesive and stimulatory events so critical to the extravasation of neutrophils from postcapillary venules in many tissues is not evident in this setting. Compelling evidence exists for unique cascades of biophysical, adhesive, stimulatory, and guidance factors that arrest neutrophils in the alveolar capillary bed and direct their movement through the endothelium, interstitial space, and alveolar epithelium. A prominent path accessible to the neutrophil appears to be determined by the structural interactions of endothelial cells, interstitial fibroblasts, as well as type I and type II alveolar epithelial cells.

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Section: B Preexisting Holes In the Basement Membranementioning

confidence: 74%

Section: Neutrophil Migration Across Vascular Endotheliummentioning

confidence: 98%

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Burns

Smith²,

Walker³

2003

Physiological Reviews

266

273

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“…PECAM-1 is also known to act on leukocyte migration but has rather been documented to halt leukocyte emigration, as PECAM-1 knockout animals have enhanced immune cell infiltration into the CNS [90]. ICAM-1 and PECAM-1 are enriched in lipid rafts and signal through lipid raft platforms provided by membrane rafts [58,91,92]. The association of CAMs with cholesterol-enriched membrane microdomains is important for optimal signal transduction events during Fig.…”

Section: Adhesion Raftsmentioning

confidence: 99%

Functions of lipid raft membrane microdomains at the blood–brain barrier

et al. 2009

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The blood-brain barrier (BBB) is a highly specialized structural and functional component of the central nervous system that separates the circulating blood from the brain and spinal cord parenchyma. Brain endothelial cells (BECs) that primarily constitute the BBB are tightly interconnected by multiprotein complexes, the adherens junctions and the tight junctions, thereby creating a highly restrictive cellular barrier. Lipid-enriched membrane microdomain compartmentalization is an inherent property of BECs and allows for the apicobasal polarity of brain endothelium, temporal and spatial coordination of cell signaling events, and actin remodeling. In this manuscript, we review the role of membrane microdomains, in particular lipid rafts, in the BBB under physiological conditions and during leukocyte transmigration/diapedesis. Furthermore, we propose a classification of endothelial membrane microdomains based on their function, or at least on the function ascribed to the molecules included in such heterogeneous rafts: (1) rafts associated with interendothelial junctions and adhesion of BECs to basal lamina (scaffolding rafts); (2) rafts involved in immune cell adhesion and migration across brain endothelium (adhesion rafts); (3) rafts associated with transendothelial transport of nutrients and ions (transporter rafts).

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“…fractions Triton X-100 soluble and insoluble fractions were prepared from cell lysate ( 2 · 10 6 HUVECs) according to Amos et al [21]. The purity of detergent soluble/insoluble fractions was verified by detecting the presence of intercellular cell adhesion molecule-1 (ICAM-1) using Western blot assay (data not shown) as ICAM-1 is known predominantly presents in the soluble fraction only [21].…”

Section: Preparation Of Detergent-soluble and Insoluble (Cytoskeleton)mentioning

confidence: 99%

“…The purity of detergent soluble/insoluble fractions was verified by detecting the presence of intercellular cell adhesion molecule-1 (ICAM-1) using Western blot assay (data not shown) as ICAM-1 is known predominantly presents in the soluble fraction only [21].…”

Section: Preparation Of Detergent-soluble and Insoluble (Cytoskeleton)mentioning

confidence: 99%

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

Wei¹,

Lü²,

Song³

et al. 2005

FEBS Letters

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The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are known to inhibit leukocyte recruitment to endothelium but the mechanism is less understood. Platelet endothelial cell adhesion molecule-1 (PECAM-1) is an endothelial junction protein involved in leukocyte diapedesis. We hypothesize that in endothelial cells, statins may well recruit PECAM-1 to exert their inhibitory effect on leukocyte transendothelial migration (TEM). In lovastatin-treated resting human umbilical vein endothelial cells (HUVECs), increased levels of mRNA and protein of PECAM-1 as well as its bio-synthesis (all 2-fold) were observed by real-time PCR, Western blotting and 35 S-labeled methionine incorporation assay, respectively. Moreover, in lovastatin treated resting cells as well as TNF-a activated endothelial cells, unanimously decreased Triton X-100 insoluble and soluble PECAM-1 ratio was observed. Such changes were accompanied by decreased TEM of U-937 cells (a promonocyte cell line). All lovastatinÕs effects were abrogated by mevalonic acid. In resting HUVECs, geranylgeranyl pyrophosphate (GGPP), but not farnesyl pyrophosphate (FPP) (both are isoprenoid intermediates in the cholesterol biosynthesis pathway) compromised the effect of lovastatin on PECAM-1 expression, whereas C3 toxin, an inhibitor of small G proteins, exerted statin-like effect.Conclusion: Statin-reduced endothelial permeability could be attributed to altered intracellular distribution of PECAM-1 in endothelial cells. We speculate that lovastatin regulates PE-CAM-1 expression in HUVECs through the mevalonate-GGPP pathway by inhibiting of Rho small GTPase.

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Cross-Linking of Brain Endothelial Intercellular Adhesion Molecule (ICAM)-1 Induces Association of ICAM-1 With Detergent-Insoluble Cytoskeletal Fraction

Cited by 33 publications

References 22 publications

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Unique Structural Features That Influence Neutrophil Emigration Into the Lung

Functions of lipid raft membrane microdomains at the blood–brain barrier

Statin‐inhibited endothelial permeability could be associated with its effect on PECAM‐1 in endothelial cells

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