- Prof. Marc F. Hoylaerts, PhD
- Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, University of Leuven, Leuven, Belgium.
Website | E-mail
Special Issue Introduction
The inner surface of blood vessels in contact with circulating blood is lined with endothelial cells. These maintain vascular integrity by preventing inappropriate adhesion and penetration of circulating leukocytes and platelets in the vascular media, adventitia and underlying tissue via modulating the activity status of blood cells. Furthermore, via an intricate anticoagulant system, the endothelium balances procoagulant signals, thus contributing to haemostasis. Disruption of this dynamic equilibrium by vascular injuries or thrombo-inflammatory stimuli activates various processes in circulating leukocytes and platelets, but also in the vasculature, affecting cell adhesion and diapedesis, platelet aggregation and coagulation activation. The endothelium surrounding mildly injured areas dampens these processes in time and space, a.o. via vascular contraction and anticoagulant activity, ultimately triggering wound healing and repair.
Genetic deficiencies have clarified how cellular receptors, signal molecules, activation processes, microRNAs and gene transcription all cooperate to achieve cardiovascular integrity. The chronic monocyte infiltration at vascular atherogenesis predilection sites revealed how long-lasting chronic inflammation modifies the infiltrated monocyte phenotype into foam cells. Such cells accumulate cholesterol, leading to atherosclerotic tissue degeneration and plaque formation, in turn linked to stenosis of a.o. coronary blood vessels, to vascular thickening and aneurysm formation.
Both platelets and endothelial cells are involved in thrombo-inflammation and atherosclerosis, via adhesion molecules and via rosette formation between leukocytes and platelets (heteroconjugates). In arterial blood vessels, smooth muscle cell activity influences blood pressure (hypertension), via (dys)regulation of several receptors and cascades. Many adhesion molecules and receptors play a role in these interactions, ranging from selectins, surface integrins, Ig-CAMS, with various receptors and adhesion molecules being expressed both by platelets and endothelial cells. Well-recognized activation cascades activate secondary platelet receptors (e.g. for ADP, thrombin, VWF, fibrinogen) and function modifiers, such as thrombospondin-1, Gas6, its 3 receptors and PEAR1 assure fine-tuning of platelet activation. NET formation by granulocytes actively contributes to thrombo-inflammatory disease in various organs, including the brain.
Some vascular receptors are still elusive (e.g., PEAR1 in endothelial cells), as are regulatory post-activation processes of thrombus maintenance and dissolution and in revascularization. This issue will focus on “bridging” explanatory reviews, and on innovative insights on (dys)function of traditional and novel receptors, their ligands and activation cascades, including (genetic) disease, relevant for vascular cells.
KeywordsEndothelial cells, platelets, leukocytes, adhesion receptors, vascular inflammation, cell activation, platelet aggregation, coagulation, anticoagulation, thrombosis, haemostasis, signaling, vascular bed
Submission Deadline15 Jun 2022