The glycocalyx and calcium dynamics in endothelial cells

Mortazavi, Cameron M.; Hoyt, Jillian M.; Patel, Aamir; Chignalia, Andréia Z.

doi:10.1016/bs.ctm.2023.02.002

Cited by 3 publications

(1 citation statement)

References 57 publications

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“…The major components of the endothelial glycocalyx that project into the vascular lumen are also involved in flow-mediated “mechanosensation-mechanotranduction” that affects nitric oxide synthesis and vasodilation [ 16 ]. In addition, the glycocalyx is involved in endothelial cell calcium dynamics as the mechanotransduction processes are mediated by the glycocalyx components are believed to either increase the calcium permeability into the cells or its release from the endoplasmic reticulum reservoirs [ 17 ]. The mechanotransduction of the luminal shear stress due to the increased blood flow into various chemical processes in the endothelial cells, involves the interaction of the glycocalyx with both membrane and cytoskeletal proteins [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Glycocalyx–Sodium Interaction in Vascular Endothelium

Sembajwe,

Ssekandi,

Namaganda

et al. 2023

Nutrients

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The glycocalyx generally covers almost all cellular surfaces, where it participates in mediating cell-surface interactions with the extracellular matrix as well as with intracellular signaling molecules. The endothelial glycocalyx that covers the luminal surface mediates the interactions of endothelial cells with materials flowing in the circulating blood, including blood cells. Cardiovascular diseases (CVD) remain a major cause of morbidity and mortality around the world. The cardiovascular risk factors start by causing endothelial cell dysfunction associated with destruction or irregular maintenance of the glycocalyx, which may culminate into a full-blown cardiovascular disease. The endothelial glycocalyx plays a crucial role in shielding the cell from excessive exposure and absorption of excessive salt, which can potentially cause damage to the endothelial cells and underlying tissues of the blood vessels. So, in this mini review/commentary, we delineate and provide a concise summary of the various components of the glycocalyx, their interaction with salt, and subsequent involvement in the cardiovascular disease process. We also highlight the major components of the glycocalyx that could be used as disease biomarkers or as drug targets in the management of cardiovascular diseases.

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Section: Introductionmentioning

confidence: 99%

Glycocalyx–Sodium Interaction in Vascular Endothelium

Sembajwe,

Ssekandi,

Namaganda

et al. 2023

Nutrients

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Ca2+ transients on the T cell surface trigger rapid integrin activation in a timescale of seconds

Li,

Wang,

Zhang

et al. 2024

Nat Commun

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One question in lymphocyte homing is how integrins are rapidly activated to enable immediate arrest of fast rolling lymphocytes upon encountering chemokines at target vascular beds given the slow chemokine-induced integrin inside-out activation. Herein we demonstrate that chemokine CCL25-triggered Ca2+ influx induces T cell membrane-proximal external Ca2+ concentration ([Ca2+]ex) drop in 6 s from physiological concentration 1.2 mM to 0.3 mM, a critical extracellular Ca2+ threshold for inducing αLβ2 activation, triggering rapid αLβ2 activation and T cell arrest before occurrence of αLβ2 inside-out activation. Talin knockdown inhibits the slow inside-out activation of αLβ2 but not [Ca2+]ex drop-triggered αLβ2 quick activation. Blocking Ca2+ influx significantly suppresses T cell rolling-to-arrest transition and homing to skin lesions in a mouse psoriasis model, thus alleviating skin inflammation. [Ca2+]ex decrease-triggered rapid integrin activation bridges the gap between initial chemokine stimulation and slow integrin inside-out activation, ensuring immediate lymphocyte arrest and subsequent diapedesis on the right location.

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Pathophysiological basis of hepatopulmonary syndrome

Chooklin,

Chuklin,

Posivnych

et al. 2024

GASTRO

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Circulatory changes with increased blood flow and vasodilatation/vasoconstriction imbalance are an integral consequence of liver cirrhosis and portal hypertension and can affect the pulmonary circulation with the development of vascular disorders, with hepatopulmonary syndrome (HPS) being the most common. HPS is a serious pulmonary complication of progressive liver disease, resulting in a poor clinical prognosis. Vascular tone decrease, monocytic infiltration of pulmonary vessels, formation of intrapulmonary arteriovenous shunts, dysfunction of alveolar type II cells, destruction of the endothelial glycocalyx are important in the pathogenesis of HPS. Abnormalities of pulmonary capillaries lead to hypoxemia caused by a violation of the ventilation/perfusion ratio, diffusion disorders, and the development of arteriovenous anastomoses. Infiltration of the pulmonary vessels by monocytes is one of the key factors of HPS. This migration is facilitated by the intestinal microbiota translocation into the portal bloodstream with increased expression of proinflammatory cytokines (tumor necrosis factor α, interleukins 1, 6), leading to the activation of monocytes. Monocytes located in the pulmonary circulation promote the vasodilation through the activation of inducible nitric oxide (NO) synthase and thus NO production. This is also associated with endothelial dysfunction due to a decreased hepatic secretion of bone morphogenetic protein 9 and increased endothelin 1, endothelial overexpression of endothelin B receptors, and increased endothelial NO production. Proangiogenic factors such as vascular endothelial growth factor, platelet-derived growth factor, and placental growth factor play an important role in the proliferation of pulmonary capillaries. Circulation of tumor necrosis factor α, bile acids and monocyte infiltration in the pulmonary circulation lead to increased apoptosis of alveolar type II cells and decreased surfactant synthesis. Chronic inflammation in HPS disrupts the continuity of the endothelial glycocalyx layer. This article provides an overview of the current knowledge on the pathogenesis of HPS, summarizes many features of the disease based on the literature research in MEDLINE database on the PubMed platform.

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The glycocalyx and calcium dynamics in endothelial cells

Cited by 3 publications

References 57 publications

Glycocalyx–Sodium Interaction in Vascular Endothelium

Glycocalyx–Sodium Interaction in Vascular Endothelium

Ca2+ transients on the T cell surface trigger rapid integrin activation in a timescale of seconds

Pathophysiological basis of hepatopulmonary syndrome

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