Abstract
Caveolins are involved in anaesthetic-induced cardioprotection. Actin filaments are located in close connection to Caveolins in the plasma membrane. We hypothesised that helium might affect the cytoskeleton and induce secretion of Caveolin. HCAEC, HUVEC and Cav-1 siRNA transfected HUVEC were exposed for 20 minutes to either helium (5% CO2, 25% O2, 70% He) or control gas (5% CO2, 25% O2, 70% N2). Cells and supernatants were collected for infrared Western blot analysis, immunofluorescence staining, nanoparticle tracking analysis and permeability measurements. Helium treatment increased the cortical localisation of F-actin fibers in HUVEC. After 6 hours, helium decreased cellular Caveolin-1 (Cav-1) levels and increased Cav-1 levels in the supernatant. Cell permeability was decreased 6 and 12 hours after helium treatment, and increased levels of Vascular Endothelial - Cadherin (VE-Cadherin) and Connexin 43 (Cx43) were observed. Transfection with Cav-1 siRNA abolished the effects of helium treatment on VE-Cadherin, Cx43 levels and permeability. Supernatant obtained after helium treatment reduced cellular permeability in remote HUVEC, indicating that increased levels of Cav-1 are responsible for the observed alterations. These findings suggest that Cav-1 is secreted after helium exposure in vitro, altering the cytoskeleton and increasing VE-Cadherin and Cx43 expression resulting in decreased permeability in HUVEC.
Highlights
The non-anaesthetic noble gas helium induces both pre- and postconditioning in vivo and in vitro, protecting against subsequent prolonged ischaemia of an organ
To get more insights into the protective effect of helium on a cellular level, the effect of helium on cellular actin filament alignment was assessed by actin staining of treated human umbilical vein endothelial cells (HUVEC)
The major findings of this study are that exposure to the noble gas helium causes structural alterations to the cytoskeleton that preserve membrane stability and decrease vascular permeability in venous endothelial cells
Summary
The non-anaesthetic noble gas helium induces both pre- and postconditioning in vivo and in vitro, protecting against subsequent prolonged ischaemia of an organ. Several mediators behind helium conditioning were described, radical oxygen scavengers, the mitochondrial adenosine triphosphate regulated potassium channel (KATP)[4], and the calcium sensitive potassium channel play a role in helium induced protection[5,6]. These mediators are all located on the mitochondrial membrane, probably indicating that the key mechanism behind helium conditioning congregates on this level. Conditioning in mice resulted in a decreased level of Caveolin-1 (Cav-1) and -3 in the heart, with a concomitant increase of Cav-1 and -3 levels in the blood, suggesting that circulating factors in the blood are involved in helium induced organ protection[13]. Preconditioning preserves sarcolemmal Cx43 activity during sustained ischaemia, leading to maintenance of cellular integrity and decreasing cellular edema[23]
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