Bases cellulaires de la mécanotransduction dans la cellule endothéliale

Lehoux, Stéphanie; Tedgui, Alain

doi:10.1051/medsci/2004205551

Cited by 13 publications

(3 citation statements)

References 38 publications

(41 reference statements)

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“…ECs possess numerous mechanoreceptors responding to flow, 24,37,62 including PECAM itself. 41 Acute shear stress generates tension between adjacent endothelial cells and causes phosphorylation of PECAM cytoplasmic tail, initiating flow-mediated intracellular signaling pathways.…”

Section: Resultsmentioning

confidence: 99%

Acute and Chronic Shear Stress Differently Regulate Endothelial Internalization of Nanocarriers Targeted to Platelet-Endothelial Cell Adhesion Molecule-1

Han¹,

Zern²,

Shuvaev³

et al. 2012

ACS Nano

103

118

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Intracellular delivery of nanocarriers (NC) is controlled by their design and target cell phenotype, microenvironment, and functional status. Endothelial cells (EC) lining the vascular lumen represent an important target for drug delivery. Endothelium in vivo is constantly or intermittently (as, for example, during ischemia-reperfusion) exposed to blood flow, which influences NC–EC interactions by changing NC transport properties, and by direct mechanical effects upon EC mechanisms involved in NC binding and uptake. EC do not internalize antibodies to marker glycoprotein PECAM(CD31), yet internalize multivalent NC coated with PECAM antibodies (anti-PECAM/NC) via a noncanonical endocytic pathway distantly related to macropinocytosis. Here we studied the effects of flow on EC uptake of anti-PECAM/NC spheres (∼180 nm diameter). EC adaptation to chronic flow, manifested by cellular alignment with flow direction and formation of actin stress fibers, inhibited anti-PECAM/NC endocytosis consistent with lower rates of anti-PECAM/NC endocytosis in vivo in arterial compared to capillary vessels. Acute induction of actin stress fibers by thrombin also inhibited anti-PECAM/NC endocytosis, demonstrating that formation of actin stress fibers impedes EC endocytic machinery. In contrast, acute flow without stress fiber formation, stimulated anti-PECAM/NC endocytosis. Anti-PECAM/NC endocytosis did not correlate with the number of cell-bound particles under flow or static conditions. PECAM cytosolic tail deletion and disruption of cholesterol-rich plasmalemma domains abrogated anti-PECAM/NC endocytosis stimulation by acute flow, suggesting complex regulation of a flow-sensitive endocytic pathway in EC. The studies demonstrate the importance of the local flow microenvironment for NC uptake by the endothelium and suggest that cell culture models of nanoparticle uptake should reflect the microenvironment and phenotype of the target cells.

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Section: Resultsmentioning

confidence: 99%

Acute and Chronic Shear Stress Differently Regulate Endothelial Internalization of Nanocarriers Targeted to Platelet-Endothelial Cell Adhesion Molecule-1

Han¹,

Zern²,

Shuvaev³

et al. 2012

ACS Nano

103

118

View full text Add to dashboard Cite

show abstract

“…A low and/or oscillating shear stress can cause the endothelial cells to become pro-inflammatory, apoptotic, more proliferative, prothrombotic or unable to regulate vascular tone [27]. In vivo, these mechanisms are responsible for vascular remodelling via smooth muscle cells which are sensitive to stretch and ECs which are sensitive to stretch and shear stress [28]. However, stresses could exceed a healthy threshold during frictional interaction.…”

Section: Tribology and Endothelial Cells: Friction Induced Effects On...mentioning

confidence: 99%

Bio-tribology of Vascular Devices: A Review of Tissue/Device Friction Research

et al. 2021

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“…It has been argued in the literature that data obtained in vitro using static binding assays may not be relevant to the fluid dynamic environment encountered in the vasculature (99). There are a growing number of papers in the literature in the last number of years suggesting that the local fluid environment of the circulation critically affects the molecular pathways of cell–cell interactions (100, 101). Platelets perfused over immobilised S. sanguinis or S. gordonii interacted with a typical rolling behaviour followed by firm adhesion.…”

Section: The Interaction Between Streptococci and Plateletsmentioning

confidence: 99%

The thrombotic potential of oral pathogens

Kerrigan

Cox

2009

Journal of Oral Microbiology

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In recent times the concept of infectious agents playing a role in cardiovascular disease has attracted much attention. Chronic oral disease such as periodontitis, provides a plausible route for entry of bacteria to the circulation. Upon entry to the circulation, the oral bacteria interact with platelets. It has been proposed that their ability to induce platelet aggregation and support platelet adhesion is a critical step in the pathogenesis of the infection process. Many published studies have demonstrated multiple mechanisms through which oral bacteria are able to bind to and activate platelets. This paper will review the various mechanisms oral bacteria use to interact with platelets.

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Bases cellulaires de la mécanotransduction dans la cellule endothéliale

Cited by 13 publications

References 38 publications

Acute and Chronic Shear Stress Differently Regulate Endothelial Internalization of Nanocarriers Targeted to Platelet-Endothelial Cell Adhesion Molecule-1

Acute and Chronic Shear Stress Differently Regulate Endothelial Internalization of Nanocarriers Targeted to Platelet-Endothelial Cell Adhesion Molecule-1

Bio-tribology of Vascular Devices: A Review of Tissue/Device Friction Research

The thrombotic potential of oral pathogens

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