Plasma membrane wound repair is characterized by extensive membrane lipid and protein rearrangements in vascular endothelial cells

2021 ◽  
pp. 118991
Author(s):  
Arsila P.K. Ashraf ◽  
Volker Gerke
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Wound Repair ◽  
Vascular Endothelial Cells ◽  
Membrane Lipid ◽  
Vascular Endothelial

scholarly journals Mechanotransduction in an extracted cell model: Fyn drives stretch- and flow-elicited PECAM-1 phosphorylation

2008 ◽  
Vol 182 (4) ◽  
pp. 753-763 ◽  
Author(s):  
Yi-Jen Chiu ◽  
Elena McBeath ◽  
Keigi Fujiwara
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Adhesion Molecule ◽  
Mammalian Cells ◽  
Kinase Inhibitors ◽  
Vascular Endothelial Cells ◽  
Cell Model ◽  
Vascular Endothelial ◽  
Small Interfering Rnas ◽  
Essential Components

Mechanosensing followed by mechanoresponses by cells is well established, but the mechanisms by which mechanical force is converted into biochemical events are poorly understood. Vascular endothelial cells (ECs) exhibit flow- and stretch-dependent responses and are widely used as a model for studying mechanotransduction in mammalian cells. Platelet EC adhesion molecule 1 (PECAM-1) is tyrosine phosphorylated when ECs are exposed to flow or when PECAM-1 is directly pulled, suggesting that it is a mechanochemical converter. We show that PECAM-1 phosphorylation occurs when detergent-extracted EC monolayers are stretched, indicating that this phosphorylation is mechanically triggered and does not require the intact plasma membrane and soluble cytoplasmic components. Using kinase inhibitors and small interfering RNAs, we identify Fyn as the PECAM-1 kinase associated with the model. We further show that stretch- and flow-induced PECAM-1 phosphorylation in intact ECs is abolished when Fyn expression is down-regulated. We suggest that PECAM-1 and Fyn are essential components of a PECAM-1–based mechanosensory complex in ECs.

A mathematical model of plasma membrane electrophysiology and calcium dynamics in vascular endothelial cells

2007 ◽  
Vol 293 (1) ◽  
pp. C277-C293 ◽  
Author(s):  
Haroldo S. Silva ◽  
Adam Kapela ◽  
Nikolaos M. Tsoukias
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Plasma Membrane ◽  
Vascular Tone ◽  
Vascular Endothelial Cells ◽  
Anion Channel ◽  
Ionic Species ◽  
Vascular Endothelial ◽  
Health And Disease ◽  
Vascular Autoregulation

Vascular endothelial cells (ECs) modulate smooth muscle cell (SMC) contractility, assisting in vascular tone regulation. Cytosolic Ca2+ concentration ([Ca2+]i) and membrane potential ( Vm) play important roles in this process by controlling EC-dependent vasoactive signals and intercellular communication. The present mathematical model integrates plasmalemma electrophysiology and Ca2+ dynamics to investigate EC responses to different stimuli and the controversial relationship between [Ca2+]i and Vm. The model contains descriptions for the intracellular balance of major ionic species and the release of Ca2+ from intracellular stores. It also expands previous formulations by including more detailed transmembrane current descriptions. The model reproduces Vm responses to volume-regulated anion channel (VRAC) blockers and extracellular K+ concentration ([K+]o) challenges, predicting 1) that Vm changes upon VRAC blockade are [K+]o dependent and 2) a biphasic response of Vm to increasing [K+]o. Simulations of agonist-induced Ca2+ mobilization replicate experiments under control and Vm hyperpolarization blockade conditions. They show that peak [Ca2+]i is governed by store Ca2+ release while Ca2+ influx (and consequently Vm) impacts more the resting and plateau [Ca2+]i. The Vm sensitivity of rest and plateau [Ca2+]i is dictated by a [Ca2+]i “buffering” system capable of masking the Vm-dependent transmembrane Ca2+ influx. The model predicts plasma membrane Ca2+-ATPase and Ca2+ permeability as main players in this process. The heterogeneous Vm impact on [Ca2+]i may elucidate conflicting reports on how Vm influences EC Ca2+. The present study forms the basis for the development of multicellular EC-SMC models that can assist in understanding vascular autoregulation in health and disease.

scholarly journals Ectoadenylate Kinase and Plasma Membrane ATP Synthase Activities of Human Vascular Endothelial Cells

2006 ◽  
Vol 281 (30) ◽  
pp. 20728-20737 ◽  
Author(s):  
Ellen E. Quillen ◽  
Gale C. Haslam ◽  
Hardeep S. Samra ◽  
Darius Amani-Taleshi ◽  
Jeffrey A. Knight ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Atp Synthase ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

Inhibition by antisense oligonucleotides of plasma membrane Ca2+ ATPase in vascular endothelial cells

2000 ◽  
Vol 387 (3) ◽  
pp. 273-277 ◽  
Author(s):  
Miki Nakao ◽  
Ken-Ichi Furukawa ◽  
Eisaku Satoh ◽  
Kyoichi Ono ◽  
Toshihiko Iijima
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Antisense Oligonucleotides ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Autophagy regulates hyaluronan synthase 2 levels in vascular endothelial cells

2018 ◽  
Author(s):  
Carolyn G. Chen ◽  
Maria A. Gubbiotti ◽  
Xiaorui Han ◽  
Yanglei Yu ◽  
Robert J. Linhardt ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Wound Repair ◽  
Vascular Endothelial Cells ◽  
Hyaluronan Synthase ◽  
Vascular Endothelial ◽  
Hyaluronan Synthases ◽  
Main Driver ◽  
Tumor Neovascularization ◽  
Core Components ◽  
Hyaluronan Synthase 2

AbstractHyaluronan is emerging as a key player regulating wound repair, inflammation, and angiogenesis. Of the three hyaluronan synthases (HAS1-3), HAS2 is the main driver of tumorigenicity by enhancing hyaluronan deposition. We discovered that HAS2 was degraded in vascular endothelial cells via autophagy, a catabolic process evoked by endorepellin and endostatin, two angiostatic and pro-autophagic effectors, and by Torin 1, a specific mTOR inhibitor. Protracted autophagy increased co-localization of HAS2 with three core components of the autophagosome, LC3, p62, and ATG9A, and binding of HAS2 to ATG9A. Importantly, autophagic induction led to an exclusive and marked suppression of secreted hyaluronan with no significant effects on either heparan or chondroitin sulfate levels. Thus, we have unveiled autophagy as a key catabolic mechanism regulating the production of hyaluronan in endothelial cells. Moreover, our study provides a biological link between autophagy and angiogenesis that could lead to potential targets for tumor neovascularization.SummaryHyaluronan is pro-angiogenic and pro-tumorigenic. We report a novel mechanism through which three autophagic inducers―endorepellin, endostatin, and Torin 1―regulate the levels of hyaluronan synthase-2. Protracted autophagy results in suppression of extracellular hyaluronan, thereby implicating autophagy in the regulation hyaluronan production.

scholarly journals Localization of rat endothelin-converting enzyme to vascular endothelial cells and some secretory cells

1995 ◽  
Vol 311 (2) ◽  
pp. 657-665 ◽  
Author(s):  
M Takahashi ◽  
K Fukuda ◽  
K Shimada ◽  
K Barnes ◽  
A J Turner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Vascular Endothelial Cells ◽  
Simian Virus 40 ◽  
Secretory Cells ◽  
Rat Tissues ◽  
Vascular Endothelial ◽  
Converting Enzyme ◽  
Reducing Conditions ◽  
Endothelin Converting Enzyme

Endothelin is a potent vasoconstrictive peptide that is produced by vascular endothelial cells; it is formed from its precursor, big endothelin, by endothelin-converting enzyme (ECE). In this work, ECE was studied using specific monoclonal antibodies. In immunoblotting, ECE was estimated to be a 300 kDa protein on SDS/PAGE under non-reducing conditions, and 130 kDa under reducing conditions. Cross-linking experiments revealed that ECE is composed of two disulphide-linked subunits. Localization of ECE was studied at the cellular and subcellular levels in various rat tissues and cells. High-level expression of ECE was observed in membrane fractions of simian virus 40-transformed rat endothelial cells by immunoblotting, but the immunoreactive band was absent form aortic smooth muscle cells and cytosolic fractions of endothelial cells. In immunohistochemical analysis, ECE was found to be localized in the endothelial cells of the aorta, lung, kidney, liver and heart. Confocal immunofluorescent microscopy showed that most of the ECE in endothelial cells and cells transfected with ECE cDNA was clustered along the plasma membrane. Intact COS or CHO cells transfected with ECE cDNA rapidly and efficiently cleaved big endothelin-1 added to the culture medium. Thus endothelial cells express ECE on the plasma membrane and the active site of the enzyme faces outside the cells, i.e. it is an ectoenzyme. Other than endothelial cells, ECE was also present in some secretory cells. The enzyme was abundant in the adrenal gland, and localized in chromaffin cells. ECE was also highly condensed in pancreatic islet beta cells. It is concluded that ECE and endothelin may be involved in the regulated secretion of hormones.

Plasma membrane-dependent activation of gelatinase A in human vascular endothelial cells

1995 ◽  
Vol 165 (3) ◽  
pp. 475-483 ◽  
Author(s):  
J. M. Lewalle ◽  
C. Munaut ◽  
B. Pichot ◽  
D. Cataldo ◽  
E. Baramova ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Gelatinase A

Cytotoxicity and Genotoxic Effects of Organic Extracts from Traffic-Related Particulate Matter in Human Vascular Endothelial Cells

2012 ◽  
Vol 610-613 ◽  
pp. 686-690
Author(s):  
Yu Shang ◽  
Lan Lan Fan ◽  
Ling Zhang
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Endothelial Cells ◽  
Plasma Membrane ◽  
Particulate Matter ◽  
Vascular Endothelial Cells ◽  
Membrane Damage ◽  
Cell Culture Supernatant ◽  
Vascular Endothelial ◽  
Organic Extracts

Traffic-related particulate matter (PM) is associated with adverse cardiovascular effects. However, the direct impact of the traffic-related PM on the cytotoxicity and genotoxic damage in vascular endothelial cells is less well known. The aim of the present study is to assess whether exposure to the organic extracts of traffic related-PM (oTRP) can induce cytotoxicity, DNA damage and oxidative stress in the human umbilical vein endothelial cells (HUVEC). The cell viability was determined by MTT assay after treatment with oTRP for 24 h. The injury of the cell plasma membrane was evaluated by testing the lactate dehydrogenase (LDH) leakage in cell culture supernatant. The activity of superoxide dismutase (SOD) was determined to evaluate the level of oxidative stress in cells. DNA damage was measured by alkaline Comet assay. The results showed that significantly dose-dependent cytotoxicity and DNA damage was detected in HUVEC after treated with oTRP for 24 h. A concomitant decrease in SOD activity was observed, suggesting that oTRP may mediate genotoxic and cytotoxic effects in HUVEC through the oxidative stress pathway. These results indicate that organic extracts of traffic related-PM has a potency to cause oxidative stress, DNA damage, cell death and plasma membrane damage in HUVEC, thus may be participated in the development of cardiovascular diseases through damaging vascular endothelial cells.

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