The effects of hyperoxia on microvascular endothelial cell proliferation and production of vaso-active substances

Attaye, Ilias; Smulders, Yvo M.; Waard, Monique C. de; Straaten, Heleen M. Oudemans–van; Smit, Bob; Wijhe, Michiel H. van; Musters, René J.P.; Koolwijk, Pieter; Man, A.M.E. Spoelstra-de

doi:10.1186/s40635-017-0135-4

Cited by 26 publications

(35 citation statements)

References 67 publications

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“…On one hand, immature rat pups exposed to F I O 2 = 0.8 for 6 h display higher nitrotyrosine staining in the apical dendrites of neurons [ 137 ] (but the PO 2 -dependent proteins nitration appears to be controlled consistently by NO concentration [ 142 ]). On the other hand, human microvascular endothelial cells cultured at F I O 2 = 0.95 for 72 h do not show appreciable changes in neither the nitrotyrosine levels nor the eNOS mRNA and protein expression levels, regardless of PO 2 [ 143 ]. Observations gathered in rats exposed to 2.8 atm show that the augmented NO synthesis is associated with increased nNOS activation, Hsp90 and intracellular calcium entry [ 144 ].…”

Section: Nitric Oxidementioning

confidence: 99%

Comparative Response of Brain to Chronic Hypoxia and Hyperoxia

Terraneo

Samaja

2017

IJMS

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Two antithetic terms, hypoxia and hyperoxia, i.e., insufficient and excess oxygen availability with respect to needs, are thought to trigger opposite responses in cells and tissues. This review aims at summarizing the molecular and cellular mechanisms underlying hypoxia and hyperoxia in brain and cerebral tissue, a context that may prove to be useful for characterizing not only several clinically relevant aspects, but also aspects related to the evolution of oxygen transport and use by the tissues. While the response to acute hypoxia/hyperoxia presumably recruits only a minor portion of the potentially involved cell machinery, focusing into chronic conditions, instead, enables to take into consideration a wider range of potential responses to oxygen-linked stress, spanning from metabolic to genic. We will examine how various brain subsystems, including energetic metabolism, oxygen sensing, recruitment of pro-survival pathways as protein kinase B (Akt), mitogen-activated protein kinases (MAPK), neurotrophins (BDNF), erythropoietin (Epo) and its receptors (EpoR), neuroglobin (Ngb), nitric oxide (NO), carbon monoxide (CO), deal with chronic hypoxia and hyperoxia to end-up with the final outcomes, oxidative stress and brain damage. A more complex than expected pattern results, which emphasizes the delicate balance between the severity of the stress imposed by hypoxia and hyperoxia and the recruitment of molecular and cellular defense patterns. While for certain functions the expectation that hypoxia and hyperoxia should cause opposite responses is actually met, for others it is not, and both emerge as dangerous treatments.

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Section: Nitric Oxidementioning

confidence: 99%

Comparative Response of Brain to Chronic Hypoxia and Hyperoxia

Terraneo

Samaja

2017

IJMS

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“…Notably, both the ICA and VA shear rate were reduced in the present study following a single SCUBA dive; as such, repeated/prolonged exposure to hyperoxia may contribute to pressure-induced reductions in microvascular endothelial integrity following chronic participation in SCUBA diving (Attaye et al, 2017;Brueckl et al, 2006). Whether prolonged exposure to hyperoxia and hyperbaria during longer, deeper, colder and/or repetitive SCUBA dives would provoke changes to the functional responses of the cerebrovasculature requires further investigation.…”

Section: Stability In Functional Cbf Regulation Following a Scuba Divementioning

confidence: 63%

“…The reasons for the alterations in extra-cranial blood flow patterns are not clear but may relate to hyperoxia-induced endotheliummediated regulation of CBF as evidenced by reductions in ICA and VA shear rate following the SCUBA dive (Attaye et al, 2017;Brueckl et al, 2006). Further, the attenuation in ICA and VA shear rates is likely influenced by the observed 19% decrease in cardiac output; these data are consistent with the 17% reduction in cardiac output 30 min following a single SCUBA dive reported by Dujic and colleagues (2005).…”

Section: Cerebrovascular Regulation At Rest Following a Scuba Divementioning

confidence: 99%

Alterations in resting cerebrovascular regulation do not affect reactivity to hypoxia, hyperoxia or neurovascular coupling following a SCUBA dive

Caldwell

Hoiland

Barak

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study?What are the characteristics of cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18 m sea water with a 47 min bottom time. What is the main finding and its importance?Acute alterations in CBF regulation at rest, including extra‐cranial vasodilatation, reductions in shear patterns and elevations in intra‐cranial blood velocity were observed at rest following a single SCUBA dive.These subtle changes in CBF regulation did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or neurovascular coupling following a single SCUBA dive. Abstract Reductions in vascular function during a SCUBA dive – due to hyperoxia‐induced oxidative stress, arterial and venous gas emboli and altered endothelial integrity – may also extend to the cerebrovasculature following return to the surface. This study aimed to characterize cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18 m sea water with a 47 min bottom time. Prior to and following the dive, participants (n = 11) completed (1) resting CBF in the internal carotid (ICA) and vertebral (VA) arteries (duplex ultrasound) and intra‐cranial blood velocity (v) of the middle and posterior cerebral arteries (MCAv and PCAv, respectively) (transcranial Doppler ultrasound); (2) cerebrovascular reactivity to acute poikilocapnic hypoxia (i.e. FnormalIO2, 0.10) and hyperoxia (i.e. FnormalIO2, 1.0); and (3) neurovascular coupling (NVC; regional CBF response to local increases in cerebral metabolism). Global CBF, cerebrovascular reactivity to hypoxia and hyperoxia, and NVC were unaltered following a SCUBA dive (all P > 0.05); however, there were subtle changes in other cerebrovascular metrics post‐dive, including reductions in ICA (−13 ± 8%, P = 0.003) and VA (−11 ± 14%, P = 0.021) shear rate, lower ICAv (−10 ± 9%, P = 0.008) and VAv (−9 ± 14%, P = 0.028), increases in ICA diameter (+4 ± 5%, P = 0.017) and elevations in PCAv (+10 ± 19%, P = 0.047). Although we observed subtle alterations in CBF regulation at rest, these changes did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or NVC. Whether prolonged exposure to hyperoxia and hyperbaria during longer, deeper, colder and/or repetitive SCUBA dives would provoke changes to the cerebrovasculature requires further investigation.

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“…Thus, because of the potential heterogeneity of the endothelial cells of the different tissues, the use of the primary endothelial cells, which were isolated from the metastatic site of interest, were to be preferred. Indeed, the studies showed significantly differed protein expression profiles in the HUVEC and endothelial cells of other origin, as well as the different behaviors of the foreskin endothelial cells versus the capillary endothelial cells from other organs [ 52 ]. While the HUVEC endothelial cells were frequently used in the model systems, the metastasis through the umbilical cord was a rare event with reliable data still lacking.…”

Section: Discussionmentioning

confidence: 99%

A Microfluidic System for the Investigation of Tumor Cell Extravasation

et al. 2018

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Metastatic dissemination of cancer cells is a very complex process. It includes the intravasation of cells into the metastatic pathways, their passive distribution within the blood or lymph flow, and their extravasation into the surrounding tissue. Crucial steps during extravasation are the adhesion of the tumor cells to the endothelium and their transendothelial migration. However, the molecular mechanisms that are underlying this process are still not fully understood. Novel three dimensional (3D) models for research on the metastatic cascade include the use of microfluidic devices. Different from two dimensional (2D) models, these devices take cell–cell, structural, and mechanical interactions into account. Here we introduce a new microfluidic device in order to study tumor extravasation. The device consists of three different parts, containing two microfluidic channels and a porous membrane sandwiched in between them. A smaller channel together with the membrane represents the vessel equivalent and is seeded separately with primary endothelial cells (EC) that are isolated from the lung artery. The second channel acts as reservoir to collect the migrated tumor cells. In contrast to many other systems, this device does not need an additional coating to allow EC growth, as the primary EC that is used produces their own basement membrane. VE-Cadherin, an endothelial adherence junction protein, was expressed in regular localization, which indicates a tight barrier function and cell–cell connections of the endothelium. The EC in the device showed in vivo-like behavior under flow conditions. The GFP-transfected tumor cells that were introduced were of epithelial or mesenchymal origin and could be observed by live cell imaging, which indicates tightly adherent tumor cells to the endothelial lining under different flow conditions. These results suggest that the new device can be used for research on molecular requirements, conditions, and mechanism of extravasation and its inhibition.

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The effects of hyperoxia on microvascular endothelial cell proliferation and production of vaso-active substances

Cited by 26 publications

References 67 publications

Comparative Response of Brain to Chronic Hypoxia and Hyperoxia

Comparative Response of Brain to Chronic Hypoxia and Hyperoxia

Alterations in resting cerebrovascular regulation do not affect reactivity to hypoxia, hyperoxia or neurovascular coupling following a SCUBA dive

A Microfluidic System for the Investigation of Tumor Cell Extravasation

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