Markers and Biomarkers of Endothelium: When Something Is Rotten in the State

Abstract

Endothelium is a community of endothelial cells (ECs), which line the blood and lymphatic vessels, thus forming an interface between the tissues and the blood or lympha. This strategic position of endothelium infers its indispensable functional role in controlling vasoregulation, haemostasis, and inflammation. The state of endothelium is simultaneously the cause and effect of many diseases, and this is coupled with modifications of endothelial phenotype represented by markers and with biochemical profile of blood represented by biomarkers. In this paper, we briefly review data on the functional role of endothelium, give definitions of endothelial markers and biomarkers, touch on the methodological approaches for revealing biomarkers, present an implicit role of endothelium in some toxicological mechanistic studies, and survey the role of reactive oxygen species (ROS) in modulation of endothelial status.

Alternative trafficking of Weibel‐Palade body proteins in CRISPR/Cas9‐engineered von Willebrand factor–deficient blood outgrowth endothelial cells

“…This suggests that these proteins are still present, although they may display alternative localizations in the absence of WPBs. The expression profiles of a select array of WPB and endothelial markers 43 presented no differences between CTRL and VWF −/− clones ( Figure 4C), establishing that apart from lacking VWF, these cells have retained their endothelial characteristics.…”

Novel Insight into Neuroimmune Regulatory Mechanisms and Biomarkers Linking Major Depression and Vascular Diseases: The Dilemma Continues

“…A healthy endothelium is characterized by a vasodilatory phenotype with high levels of nitric oxide (NO) and prostacyclin, and low levels of uric acid and reactive oxygen species (ROS). On the contrary, endothelial dysfunction is defined as a state of imbalance between the factors, with vasodilatory, antithrombogenic, and antimitogenic effects (mainly NO, prostacyclin, and endothelium-derived hyperpolarizing factor), and substances with vasoconstrictor, prothrombogenic, and proliferative effects (e.g., angiotensin II, endothelin 1, free oxygen radicals, and thromboxane) [25,26]. Thus, endothelial dysfunction predisposes the vessel wall to vasoconstriction, leukocyte adherence, platelet activation, mitogenesis, pro-oxidation, thrombosis, impaired coagulation, vascular inflammation, and atherosclerosis.…”

“…Another approach to evaluate microvascular endothelial dysfunction is based on the measurement of plasma levels of endothelium-related markers. From the aspect of endothelium principal markers, Weibel-Palade bodies are specific endothelial organelles containing von Willebrand factor (VWF), P-selectin, and angiopoetin-2, which participate in platelet binding, leukocyte recruitment, and inflammation modulation, respectively [25]. With respect to vascular pathology, endothelial damage is characterized by increased plasma levels of soluble fractions of intercellular adhesion molecule-1 (ICAM-1), or vascular-cell adhesion molecule-1 (VCAM-1) [28].…”

“…With respect to vascular pathology, endothelial damage is characterized by increased plasma levels of soluble fractions of intercellular adhesion molecule-1 (ICAM-1), or vascular-cell adhesion molecule-1 (VCAM-1) [28]. A novel list of major and minor endothelial markers with their detailed characteristics is reported in a recent review by Goncharov et al [25].…”

“…Furthermore, the high population of endothelial progenitor cells associated with low levels of endothelial microparticles and circulating endothelial cells indicates a normal function of the endothelium. Specifically, endothelial microparticles are circulating submicron-sized vesicles originated from damaged endothelial cells with various biological functions; as primary and secondary messengers of vascular inflammation, thrombosis, vasomotor response, angiogenesis, and endothelial survival [25]. Therefore, detachment of endothelial cells from the vascular wall represents another characteristic of endothelial damage, leading to a disrupted endothelium and facilitating platelets to interact with the exposed subendothelium.…”