Brain microvascular endothelial cells resist elongation due to curvature and shear stress

Ye, Mao; Sanchez, Henry; Hultz, Margot; Yang, Zhen; Bogorad, Max I.; Wong, Andrew D.; Searson, Peter C.

doi:10.1038/srep04681

Cited by 109 publications

(141 citation statements)

References 32 publications

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“…For example, HbmECs are characterized by less permissibility, absence of fenestration and high expression of tight and adherens junctions [9, 10, 44]. In addition, HbmECs display selective expression of cell adhesion molecules, higher transendothelial electrical resistance, and elongation resistance to curvature and shear stress [45–48]. Of note, both HbmECs and HUVECs show the characteristic cobblestone appearance which resembles endothelial cell morphology in vivo.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1–7) counteracts angiotensin II-induced dysfunction in cerebral endothelial cells via modulating Nox2/ROS and PI3K/NO pathways

Xiao

Zhang

et al. 2015

Experimental Cell Research

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Angiotensin (Ang) II, the main effector of the renin-angiotensin system, has been implicated in the pathogenesis of vascular diseases. Ang-(1-7) binds to the G protein-coupled Mas receptor (MasR) and can exert vasoprotective effects. We investigated the effects and underlying mechanisms of Ang-(1-7) on Ang II-induced dysfunction and oxidative stress in human brain microvascular endothelial cells (HbmECs). The pro-apoptotic activity, reactive oxygen species (ROS) and nitric oxide (NO) productions in HbmECs were measured. The protein expressions of nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2), serine/threonine kinase (Akt), endothelial nitric oxide synthase (eNOS) and their phosphorylated forms (p-Akt and p-eNOS) were examined by western blot. MasR antagonist and phosphatidylinositol-3-kinase (PI3K) inhibitor were used for receptor/pathway verification. We found that Ang-(1-7) suppressed Ang II-induced pro-apoptotic activity, ROS over-production and NO reduction in HbmECs, which were abolished by MasR antagonist. In addition, Ang-(1-7) down-regulated the expression of Nox2, and up-regulated the ratios of p-Akt/Akt and its downstream p-eNOS/eNOS in HbmECs. Exposure to PI3K inhibitor partially abrogated Ang-(1-7)-mediated protective effects in HbmECs. Our data suggests that Ang-(1-7)/MasR axis protects HbmECs from Ang II-induced dysfunction and oxidative stress via inhibition of Nox2/ROS and activation of PI3K/NO pathways.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-(1–7) counteracts angiotensin II-induced dysfunction in cerebral endothelial cells via modulating Nox2/ROS and PI3K/NO pathways

Xiao

Zhang

et al. 2015

Experimental Cell Research

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“…The mechanical cues however can also be transduced by the microfluidic channel geometry, as suggested by a study of the response of endothelial cells on various curvatures [48 ]. Within a microfluidic device, HUVEC and brain microvascular endothelial cells (HBMVEC) were grown around small glass rods with a diameter of 10 mm, mimicking the curvature found in microcapillaries.…”

Section: Vasculaturementioning

confidence: 99%

Microfluidic 3D cell culture: from tools to tissue models

Duinen

Trietsch

Joore

et al. 2015

Current Opinion in Biotechnology

439

328

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The transition from 2D to 3D cell culture techniques is an important step in a trend towards better biomimetic tissue models. Microfluidics allows spatial control over fluids in micrometer-sized channels has become a valuable tool to further increase the physiological relevance of 3D cell culture by enabling spatially controlled co-cultures, perfusion flow and spatial control over of signaling gradients. This paper reviews most important developments in microfluidic 3D culture since 2012. Most efforts were exerted in the field of vasculature, both as a tissue on its own and as part of cancer models. We observe that the focus is shifting from tool building to implementation of specific tissue models. The next big challenge for the field is the full validation of these models and subsequently the implementation of these models in drug development pipelines of the pharmaceutical industry and ultimately in personalized medicine applications.

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“…Some of these differences are captured by a theoretical model in which cell adhesion and active contractility balance the anisotropic bending stiffness of the stress fibers (18). Very recently, monolayers formed from different endothelial cell types cultured on wires were shown to exhibit cell type-dependent orientations (19).…”

mentioning

confidence: 99%

Architecture and migration of an epithelium on a cylindrical wire

Yevick

Duclos

Bonnet

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

105

116

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In a wide range of epithelial tissues such as kidney tubules or breast acini, cells organize into bidimensional monolayers experiencing an out-of-plane curvature. Cancer cells can also migrate collectively from epithelial tumors by wrapping around vessels or muscle fibers. However, in vitro experiments dealing with epithelia are mostly performed on flat substrates, neglecting this out-ofplane component. In this paper, we study the development and migration of epithelial tissues on glass wires of well-defined radii varying from less than 1 μm up to 85 μm. To uncouple the effect of out-of-plane curvature from the lateral confinement experienced by the cells in these geometries, we compare our results to experiments performed on narrow adhesive tracks. Because of lateral confinement, the velocity of collective migration increases for radii smaller than typically 20 μm. The monolayer dynamics is then controlled by front-edge protrusions. Conversely, high curvature is identified as the inducer of frequent cell detachments at the front edge, a phenotype reminiscent of the Epithelial−Mesenchymal Transition. High curvature also induces a circumferential alignment of the actin cytoskeleton, stabilized by multiple focal adhesions. This organization of the cytoskeleton is reminiscent of in vivo situations such as the development of the trachea of the Drosophila embryo. Finally, submicron radii halt the monolayer, which then reconfigures into hollow cysts.collective cell behaviors | out-of-plane curvature | epithelial tubes

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Brain microvascular endothelial cells resist elongation due to curvature and shear stress

Cited by 109 publications

References 32 publications

Angiotensin-(1–7) counteracts angiotensin II-induced dysfunction in cerebral endothelial cells via modulating Nox2/ROS and PI3K/NO pathways

Angiotensin-(1–7) counteracts angiotensin II-induced dysfunction in cerebral endothelial cells via modulating Nox2/ROS and PI3K/NO pathways

Microfluidic 3D cell culture: from tools to tissue models

Architecture and migration of an epithelium on a cylindrical wire

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