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Endothelial Cell Signaling

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Dr. Xavier Figueroa

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Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 8330025, Chile
Interests: microcirculation; endothelial cell signaling; conducted vasomotor responses; communication in the wall of resistance arteries; endothelial dysfunction; nitric oxide signaling

Special Issue Information

Dear Colleagues,

Endothelial cells play a critical role in the control and coordination of vascular function by working as a signal integration centre in the communication of diverse cell types of the circulatory system. One important mechanism of endothelial cell signaling is mediated by the release of autocrine/paracrine signals. Nitric oxide (NO), prostaglandins and ATP are widely recognized autocrine/paracrine signals that play diverse roles in the endothelial cell-mediated control of vascular function, such as the regulation of vasomotor tone, smooth muscle proliferation, platelet aggregation, vascular permeability, leucocyte transmigration and angiogenesis. Although connexin hemichannels (i.e., half of gap junction channel) and pannexin channels may contribute to the release of autocrine/paracrine signals, endothelial cell signaling also relies on direct gap junction channel-mediated communication with other cells of the vessel wall, such as smooth muscle cells, and cells that circulate in the blood stream, such as leucocytes. As cell homeostasis depends on the proper function of the vascular system, it is essential to improve and advance our understanding of the integrative regulation of vascular function by endothelial cell signaling. Therefore, original research articles, comprehensive reviews and novel communications related to the physiology, biochemistry and molecular biology of endothelial cell signalling in health and disease will be considered for this Special Issue.

Dr. Xavier Figueroa
Guest Editor

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Keywords

endothelial cell signaling
endothelial dysfunction
endothelium-dependent vasodilation
nitric oxide
myoendothelial communication
endothelial cell barrier
angiogenesis
conducted vasomotor responses

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Research

21 pages, 6912 KiB

Open AccessArticle

Palmitate Stimulates Expression of the von Willebrand Factor and Modulates Toll-like Receptors Level and Activity in Human Umbilical Vein Endothelial Cells (HUVECs)

by Agnieszka K. Seliga, Krzysztof Zabłocki and Joanna Bandorowicz-Pikuła

Int. J. Mol. Sci. 2024, 25(1), 254; https://doi.org/10.3390/ijms25010254 - 23 Dec 2023

Viewed by 765

Abstract

An increased concentration of palmitate in circulation is one of the most harmful factors in obesity. The von Willebrand factor (vWF), a protein involved in haemostasis, is produced and secreted by the vascular endothelium. An increased level of vWF in obese patients is associated with thrombosis and cardiovascular disease. The aim of this study was to investigate a palmitate effect on vWF in endothelial cells and understand the mechanisms of palmitate-activated signalling. Human umbilical vein endothelial cells (HUVECs) incubated in the presence of palmitate, exhibited an increased VWF gene expression, vWF protein maturation, and stimulated vWF secretion. Cardamonin, a Nuclear Factor kappa B (NF-κB) inhibitor, abolished the palmitate effect on VWF expression. The inhibition of Toll-like receptor (TLR) 2 with C29 resulted in the TLR4 overactivation in palmitate-treated cells. Palmitate, in the presence of TLR4 inhibitor TAK-242, leads to a higher expression of TLR6, CD36, and TIRAP. The silencing of TLR4 resulted in an increase in TLR2 level and vice versa. The obtained results indicate a potential mechanism of obesity-induced thrombotic complication caused by fatty acid activation of NF-κB signalling and vWF upregulation and help to identify various compensatory mechanisms related to TLR4 signal transduction. Full article

(This article belongs to the Special Issue Endothelial Cell Signaling)

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15 pages, 6812 KiB

Open AccessArticle

The Pulmonary Endothelial Glycocalyx Modifications in Glypican 1 Knockout Mice Do Not Affect Lung Endothelial Function in Physiological Conditions

by Lakshmi N. R. Thota, Joaquin E. Lopez Rosales, Ivan Placencia, Evgeny A. Zemskov, Paola Tonino, Ashley N. Michael, Stephen M. Black and Andreia Z. Chignalia

Int. J. Mol. Sci. 2023, 24(19), 14568; https://doi.org/10.3390/ijms241914568 - 26 Sep 2023

Viewed by 1064

Abstract

The endothelial glycocalyx is a dynamic signaling surface layer that is involved in the maintenance of cellular homeostasis. The glycocalyx has a very diverse composition, with glycoproteins, proteoglycans, and glycosaminoglycans interacting with each other to form a mesh-like structure. Due to its highly interactive nature, little is known about the relative contribution of each glycocalyx constituent to its overall function. Investigating the individual roles of the glycocalyx components to cellular functions and system physiology is challenging, as the genetic manipulation of animals that target specific glycocalyx components may result in the development of a modified glycocalyx. Thus, it is crucial that genetically modified animal models for glycocalyx components are characterized and validated before the development of mechanistic studies. Among the glycocalyx components, glypican 1, which acts through eNOS-dependent mechanisms, has recently emerged as a player in cardiovascular diseases. Whether glypican 1 regulates eNOS in physiological conditions is unclear. Herein, we assessed how the deletion of glypican 1 affects the development of the pulmonary endothelial glycocalyx and the impact on eNOS activity and endothelial function. Male and female 5–9-week-old wild-type and glypican 1 knockout mice were used. Transmission electron microscopy, immunofluorescence, and immunoblotting assessed the glycocalyx structure and composition. eNOS activation and content were assessed by immunoblotting; nitric oxide production was assessed by the Griess reaction. The pulmonary phenotype was evaluated by histological signs of lung injury, in vivo measurement of lung mechanics, and pulmonary ventilation. Glypican 1 knockout mice showed a modified glycocalyx with increased glycocalyx thickness and heparan sulfate content and decreased expression of syndecan 4. These alterations were associated with decreased phosphorylation of eNOS at S1177. The production of nitric oxides was not affected by the deletion of glypican 1, and the endothelial barrier was preserved in glypican 1 knockout mice. Pulmonary compliance was decreased, and pulmonary ventilation was unaltered in glypican 1 knockout mice. Collectively, these data indicate that the deletion of glypican 1 may result in the modification of the glycocalyx without affecting basal lung endothelial function, validating this mouse model as a tool for mechanistic studies that investigate the role of glypican 1 in lung endothelial function. Full article

(This article belongs to the Special Issue Endothelial Cell Signaling)

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