Relevant bibliographies by topics / Brain capillary endothelial cell

Academic literature on the topic 'Brain capillary endothelial cell'

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Published: 9 March 2023

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Journal articles on the topic "Brain capillary endothelial cell"

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Dehouck, B., M. P. Dehouck, J. C. Fruchart, and R. Cecchelli. "Upregulation of the low density lipoprotein receptor at the blood-brain barrier: intercommunications between brain capillary endothelial cells and astrocytes." Journal of Cell Biology 126, no. 2 (July 15, 1994): 465–73. http://dx.doi.org/10.1083/jcb.126.2.465.

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In contrast to the endothelial cells in large vessels where LDL receptors are downregulated, brain capillary endothelial cells in vivo express an LDL receptor. Using a cell culture model of the blood-brain barrier consisting of a coculture of brain capillary endothelial cells and astrocytes, we observed that the capacity of endothelial cells to bind LDL is enhanced threefold when cocultured with astrocytes. We next investigated the ability of astrocytes to modulate endothelial cell LDL receptor expression. We have shown that the lipid requirement of astrocytes increases the expression of endothelial cell LDL receptors. Experiments with dialysis membranes of different pore size showed that this effect is mediated by a soluble factor(s) with relative molecular mass somewhere between 3,500 and 14,000. Substituting astrocytes with smooth muscle cells or brain endothelium with endothelium from the aorta or the adrenal cortex did not enhance the luminal LDL receptor expression on endothelial cells, demonstrating the specificity of the interactions. This factor(s) is exclusively secreted by astrocytes cocultured with brain capillary endothelial cells, but it also upregulates the LDL receptor on other cell types. This study confirms the notion that the final fine tuning of cell differentiation is under local control.
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Dehouck, Bénédicte, Marie-Pierre Dehouck, Jean-Charles Fruchart, and Roméo Cecchelli. "Upregulation of the Low Density Lipoprotein Receptor at the Blood-Brain Barrier: Intercommunications between Brain Capillary Endothelial Cells and Astrocytes." Review & Expositor 84, no. 1 (February 1987): 465–73. http://dx.doi.org/10.1177/003463738708400125.

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In contrast to the endothelial cells in large vessels where LDL receptors are downregulated, brain capillary endothelial cells in vivo express an LDL receptor. Using a cell culture model of the blood-brain barrier consisting of a coculture of brain capillary endothelial cells and astrocytes, we observed that the capacity of endothelial cells to bind LDL is enhanced threefold when cocultured with astrocytes. We next investigated the ability of astrocytes to modulate endothelial cell LDL receptor expression. We have shown that the lipid requirement of astrocytes increases the expression of endothelial cell LDL receptors. Experiments with dialysis membranes of different pore size showed that this effect is mediated by a soluble factor(s) with relative molecular mass somewhere between 3,500 and 14,000. Substituting astrocytes with smooth muscle cells or brain endothelium with endothelium from the aorta or the adrenal cortex did not enhance the luminal LDL receptor expression on endothelial cells, demonstrating the specificity of the interactions. This factor(s) is exclusively secreted by astrocytes cocultured with brain capillary endothelial cells, but it also upregulates the LDL receptor on other cell types. This study confirms the notion that the final fine tuning of cell differentiation is under local control.
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Dehouck, Marie-Pierre, Paul Vigne, Gérard Torpier, Jean Philippe Breittmayer, Roméo Cecchelli, and Christian Frelin. "Endothelin-1 as a Mediator of Endothelial Cell–Pericyte Interactions in Bovine Brain Capillaries." Journal of Cerebral Blood Flow & Metabolism 17, no. 4 (April 1997): 464–69. http://dx.doi.org/10.1097/00004647-199704000-00012.

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Endothelial cells and pericytes are closely associated in brain capillaries. Together with astrocytic foot processes, they form the blood–brain barrier. Capillaries were isolated from bovine brain cortex. Pure populations of endothelial cells and pericytes were isolated and cultured in vitro. Polarized monolayers of endothelial cells preferentially secreted immunoreactive endothelin-1 (Et-1) at their abluminal (brain-facing) membrane. They did not express receptors for Et-1. Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments. These receptors were coupled to phospholipase C as demonstrated by intracellular calcium measurements using indo-1-loaded cells. Addition of Et-1 to pericytes induced marked changes in the cell morphology that were associated with a reorganization of F-actin and intermediate filaments. It is concluded that Et-1 is a paracrine mediator at the bovine blood–brain barrier and that capillary pericytes are target cells for endothelium-derived Et-1.
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Ladoux, Annie, and Christian Frelin. "Endothelins inhibit adenylate cyclase in brain capillary endothelial cells." Biochemical and Biophysical Research Communications 180, no. 1 (October 1991): 169–73. http://dx.doi.org/10.1016/s0006-291x(05)81271-9.

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Kaiser, Mathias, Malgorzata Burek, Stefan Britz, Frauke Lankamp, Steffi Ketelhut, Björn Kemper, Carola Förster, Christian Gorzelanny, and Francisco Goycoolea. "The Influence of Capsaicin on the Integrity of Microvascular Endothelial Cell Monolayers." International Journal of Molecular Sciences 20, no. 1 (December 30, 2018): 122. http://dx.doi.org/10.3390/ijms20010122.

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Microvascular endothelial cells are an essential part of many biological barriers, such as the blood–brain barrier (BBB) and the endothelium of the arteries and veins. A reversible opening strategy to increase the permeability of drugs across the BBB could lead to improved therapies due to enhanced drug bioavailability. Vanilloids, such as capsaicin, are known to reversibly open tight junctions of epithelial and endothelial cells. In this study, we used several in vitro assays with the murine endothelial capillary brain cells (line cEND) as a BBB model to characterize the interaction between capsaicin and endothelial tight junctions.
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Vigne, P., R. Marsault, J. P. Breittmayer, and C. Frelin. "Endothelin stimulates phosphatidylinositol hydrolysis and DNA synthesis in brain capillary endothelial cells." Biochemical Journal 266, no. 2 (March 1, 1990): 415–20. http://dx.doi.org/10.1042/bj2660415.

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Endothelin-1 (ET-1) is a novel vasoconstricting and cardiotonic peptide that is synthesized by the vascular endothelium. Bovine aortic endothelial cells which secrete ET in vitro lack membrane receptor sites for the peptide. Endothelial cells from rat brain microvessels that do not secrete ET in vitro express large amounts of high-affinity receptors for 125I-labelled ET-1 (Kd 0.8 nM). The ET receptor is recognized by sarafotoxin S6b and the different ET peptides with the following order of potency: ET-1 (Kd 0.5 nM) approximately equal to ET-2 (Kd 0.7 nM) greater than sarafotoxin S6b (Kd 27 nM) greater than ET-3 (Kd 450 nM). This structure-activity relationship is different from those found in vascular smooth muscle cells, renal cells and cardiac cells. ET-1 stimulates DNA synthesis in brain capillary endothelial cells. It is more potent than basic fibroblast growth factor. The action of ET on endothelial cells from microvessels involves phosphatidylinositol hydrolysis and intracellular Ca2+ mobilization. These observations suggest that brain endothelial cells might be an important target for ET.
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Grabb, Paul A., and Mark R. Gilbert. "Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier." Journal of Neurosurgery 82, no. 6 (June 1995): 1053–58. http://dx.doi.org/10.3171/jns.1995.82.6.1053.

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✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.
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Tewes, B. J., and H. J. Galla. "Lipid Polarity in Brain Capillary Endothelial Cells." Endothelium 8, no. 3 (2001): 207–20. http://dx.doi.org/10.3109/10623320109051566.

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Kim, Jeong A., Nam D. Tran, Shur-Jen Wang, and Mark Fisher. "Pericytes Regulate Fibrinolytic Function of Brain Capillary Endothelial Cells." Stroke 32, suppl_1 (January 2001): 359. http://dx.doi.org/10.1161/str.32.suppl_1.359-a.

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P110 Our prior work has shown that astrocytes inhibit fibrinolysis of brain capillary endothelial cells (eg, Stroke 1999:30;1671–1677). The complex cellular microenvironment at the blood-brain barrier includes pericytes, which are adjacent to and share basement membrane with brain capillary endothelial cells. We analyzed the hemostatic regulatory role of pericytes in a blood-brain barrier model consisting of human brain pericytes cultured on transwell membrane inserts with human brain capillary endothelial cells. We measured fibrinolysis proteins and function in media conditioned by 48 hour co-culture of human brain capillary endothelial cells and human brain pericytes, as well as brain capillary endothelial mono-cultures. Compared to endothelial mono-cultures, pericyte-endothelial co-cultures exhibited levels of tissue plasminogen activator (tPA) protein reduced by 50±15% (p<.05). Co-culture preparations showed 32±13% (p<.05) increase in levels of plasminogen activator inhibitor-1 (PAI-1) protein, the primary inhibitor of tPA. tPA activity of co-culture preparations was 54±17% (p<.05) of endothelial mono-culture preparations. These data demonstrate that human brain pericytes have an important hemostatic regulatory role for endothelial-dependent fibrinolysis in vitro. These findings provide further support for brain-specific hemostasis, with pericytes as well as astrocytes playing key regulatory roles.
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Coutinho, G. C., O. Durieu-Trautmann, A. D. Strosberg, and P. O. Couraud. "Catecholamines stimulate the IFN-gamma-induced class II MHC expression on bovine brain capillary endothelial cells." Journal of Immunology 147, no. 8 (October 15, 1991): 2525–29. http://dx.doi.org/10.4049/jimmunol.147.8.2525.

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Abstract The brain has been considered for a long time as an immunologically privileged site because of the lack of a true lymphatic system and the existence of several barriers that isolate it from the periphery. In the last few years, it became evident that cells in the central nervous system (astrocytes, microglial cells, and brain capillary endothelial cells) can be induced to express class II MHC and present Ag to T lymphocytes. The brain capillary endothelial cells, which are strategically located at the interface between blood and brain, could be involved in the initiation of immune responses within the brain parenchyma. We have previously characterized bovine brain capillary endothelial cells in culture and shown that they maintain in vitro a fully differentiated phenotype associated with the blood-brain barrier endothelium. In order to assess the role of these cells in the development of immune responses in the brain, we initiated the present study on the regulation of their class II MHC surface expression. Our data indicate that this expression on bovine brain capillary endothelial cells is inducible by IFN-gamma and further stimulated by catecholamines through activation of beta-adrenergic receptors. However, this latter effect is not mimicked by forskolin, theophylline, or dibutyryl-cAMP, suggesting the involvement of a cAMP-independent mechanism.
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Dissertations / Theses on the topic "Brain capillary endothelial cell"

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CAMBIANICA, ILARIA NADIA. "In vitro blood brain barrier models as a screening tool for brain targeted nanobased drug delivery systems." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/39834.

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The blood brain barrier (BBB) is a selective biological barrier located at the brain capillaries, that protects the central nervous system (CNS) by monitoring exchanges between blood and brain. The BBB controls and regulates the composition of the CNS environment and it still constitutes the main obstacle for drug delivery to the brain (Weiss N. et al., 2009). The significant scientific and industrial interest in the physiology and pathology of the BBB led to the development of vast number of in vitro BBB models. Even though no “ideal” model exists yet, some of the currently available ones are very useful to investigate permeability, transport mechanisms and cellular and molecular events which occur at the BBB level. New strategies for brain targeted drug delivery exploit endogenously expressed transporters to elicit drug passage across the BBB. Among them, nanoparticles represent a promising tool, since they are biocompatible and biodegradable, and they can be functionalized to target the BBB (De Boer A.G. and Gaillard P.J., 2007) (Beija M et al., 2012; Caruthers S.D. et al., 2007; Moghimi S.M. et al., 2005). In this study we settled in vitro BBB models to identify, with high-throughput screening, the most promising nanoliposomes (NL) for combined BBB crossing and binding of amyloid peptides, for joint therapy and diagnosis of Alzheimer’s disease (AD). Firstly, we characterized two in vitro models of BBB, based on immortalized cell lines of human and rat origin, the hCMEC/D3 and RBE4 cells, respectively. We tested the transendothelial electrical resistance (TEER) and the endothelial permeability (PE) of small hydrophilic compounds: our results, in agreement with data reported in literature, lead us to conclude that these cellular models are suitable for their employment as high-throughput screening tools. Subsequently, we tested NL mono-functionalized with three different peptides, the apolipoproteinE derived peptide (the ApoE monomer (mApoE), amino acids 141-150), its tandem dimer (dApoE) (141-150)2, and the Human Immunodeficency Virus type 1 (HIV-1) transactivator of transcription (TAT) peptide. We evaluated their uptake and PE; we selected the TAT functionalization as the best performing concerning cellular uptake, and the mApoE functionalization when considering both the internalization and PE. Once assessed the dynamics of mono-functionalized NL interactions with endothelial cells, we investigated mApoE- and dApoE-NL loading a curcumin-derivative (Re F. et al., 2011) to bind Aβ. We clearly demonstrated that the mApoE-functionalization allows a better drug cellular internalization, whereas dApoE-NL enhances drug PE at the highest extent. We then considered mApoE- and dApoE-NL exposing the Aβ targeting ligands phosphatidic acid (PA) or cardiolipin (CL), demonstrating that PA-mApoE-NL showed the highest cellular uptake and PE. We also studied TAT-NL exposing curcumin derivative3 (Airoldi C. et al., 2011) for Aβ binding, clearly indicating that TAT functionalization increased cellular uptake and PE of curcumin derivative3-NL. We also studied intracellular fate of NL double functionalized, exposing Aβ targeting ligands, and no co-localization was detected with acidic cellular compartments, suggesting that NL may escape from lysosomal degradative pathway. Taken together, these results indicate that the formulations herein analyzed are suitable tools for brain targeted drug and contrast agent delivery. We suggest further development of mApoE and dApoE-NL entrapped with a drug payload for their employment as BBB endothelial cell or brain targeted drug delivery tools, respectively. We also selected PAmApoE-NL and curcumin derivative3-TAT-NL as promising tools for their employment in combination for AD therapy and diagnosis. Further studies, based also on in vivo experiments, are needed to evaluate NL suitability for clinical exploitation. Finally, we inquired the endocytic mechanisms that mediates the entry of NL in the endothelial cells of BBB. We employed RNA interference technique to down-regulate caveolin1 expression. Our preliminary data suggest that caveolin1 and the related caveolaemediated endocytosis pathway may account for 40% of mApoE-NL cellular uptake. Future directions regard the down-regulation of other proteins specifically involved in different endocytic mechanisms, i.e. clathrin-mediated and adsoprptive endocytosis, in order to assess which endocytic mechanisms may account for ApoE and TAT-NL internalization.
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Nguyen, Hieu Thi Minh. "The effect of cardiolipin synthase deficiency on the mitochondrial function and barrier properties of human cerebral capillary endothelial cells." Elsevier, 2014. http://hdl.handle.net/1993/30184.

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The blood brain barrier (BBB), formed by endothelial cells lining the lumen of the brain capillaries, is a restrictively permeable interface that only allows transport of specific compounds into the brain. Cardiolipin (CL) is a mitochondrial- specific phospholipid known to be required for the activity and integrity of the respiratory chain. The current study examined the role of cardiolipin in maintaining an optimal mitochondrial function that may be necessary to support the barrier properties of the brain microvessel endothelial cells (BMECs). Endothelial cells have been suggested to obtain most of their energy through an-aerobic glycolysis based on studies of cells that were obtained from the peripheral vasculatures. However, here, we showed that the adult human brain capillary endothelial cell line (hCMEC/D3) appeared to produce ~60% of their basal ATP requirement through mitochondrial oxidative phosphorylation. In addition, RNAi mediated knockdown of the CL biosynthetic enzyme cardiolipin synthase (CLS), although did not grossly affect the mitochondrial coupling efficiency of the hCMEC/D3 cells, did seem to reduce their ability to increase their mitochondrial function under conditions of increased demand. Furthermore, the knockdown appeared to have acted as a metabolic switch causing the hCMEC/D3 cells to become more dependent on glycolysis. These cells also showed increase in [3H]-2-deoxyglucose uptake under a low glucose availability condition, which might have served as a mechanism to compensate for their reduced energy production efficiency. Interestingly, the increase in glucose uptake appeared correlated to an increase in [3H]-2-deoxyglucose glucose transport across the knockdown confluent hCMEC/D3 monolayers grown on Transwell® plates, which was used in our study as an in vitro model for the human BBB. This suggests that changes in the brain endothelial energy status may play a role in regulating glucose transport across the BBB. These observations, perhaps, also explain why the brain capillary endothelial cells were previously observed to possess higher mitochondrial content than those coming from non-BBB regions (Oldendorf et al. 1977).
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Howe, Grant Alexander. "Identification of Mechanisms Regulating Endothelial Cell Capillary Morphogenesis." Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26196.

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In order to effectively treat disorders whose pathology is marked by neovascularization, a better understanding of the pathways that mediate the processes involved in angiogenesis is needed. To this end we have identified two important pathways that regulate endothelial cell capillary morphogenesis, a key process in angiogenesis. We have identified the small GTPase RhoB as being induced by vascular endothelial growth factor (VEGF) in human umbilical vein endothelial cells (HUVECs). Depletion of RhoB inhibited endothelial cell VEGF - mediated migration, sprouting, and cord formation. Cells depleted of RhoB showed a marked increase in RhoA activation in response to VEGF. Defects in cord formation in RhoB - depleted cells could be partially restored through treatment with the Rho inhibitor C3 transferase or ROCK I/II inhibitors, indicating increased RhoA activity and enhanced downstream signaling from RhoA contribute to the phenotype of decreased cord formation observed in cells depleted of RhoB. Interestingly, we did not observe a significant change in RhoC activity in RhoB - depleted cells suggesting differential regulation of RhoA and RhoC by RhoB in HUVECs. We have also identified microRNA - 30b (miR - 30b) as being negatively regulated by VEGF and as being a negative regulator of HUVEC capillary morphogenesis. Overexpression of miR - 30b significantly reduced HUVEC cord formation in vitro, while inhibition of miR - 30b enhanced cord formation. Neither overexpression nor inhibition of miR - 30b affected migration or viability of endothelial cells. Interestingly, miR - 30b regulated the expression of TGFβ2 but not TGFβ1, with overexpression of miR - 30b inducing expression of TGFβ2 mRNA and protein, and inducing phosphorylaton of Smad2 , suggesting TGFβ2 produced in response to miR - 30b overexpression functions in an iii autocrine manner to stimulate HUVECs . MiR - 30b effects on TGFβ2 expression were found to be regulated to an extent by ATF2, as miR - 30b overexpressing cells exhibited increased levels of phosphorylated ATF2 , with depletion of ATF2 via siRNA resulting in inhibition of miR - 30b - induced TGFβ2 expression. Treatment of HUVECs with TGFβ2 inhibited cord formation, while TGFβ1 had no effect, indicating a major difference in how endothelial cells respond to these two related growth factors. Inhibition of TGFβ2 with a neutralizing antibody restored cord formation in miR - 30b overexpressing cells to levels similar to control cells, thus identifying TGFβ2 expression as contributing to the inhibitory effects of miR - 30b overexpression on capillary morphogenesis. Thus, we have identified two signaling pathways regulated by VEGF in HUVECs that further our understanding of the process of angiogenesis and may provide novel targets for therapeutic intervention into diseases involving angiogenesis.
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Allen, William Edward. "Antiangiogenesis : inhibitory factors affecting capillary endothelial cell growth." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282116.

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Glass, Catherine Ann. "Regulation of microvascular permeability by endothelial cell calcium." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289625.

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Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50832.pdf.

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Martinez, Bermudez Ana Katherine. "Isoprostanes in brain endothelial cell death." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21605.

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Oxygen free radicals have been implicated in several diseases including ischemic stroke, and myocardial infarction. They can trigger chain reactions like peroxidation of membrane phospholipids, leading to osmotic imbalance and cell death. Isoprostanes are stable products of lipid peroxidation that have a constrictor effect on the vasculature and bronchii. As isoprostanes are abundantly generated in tissues under oxidant stress, we have hypothesized that they could be related to endothelial dysfunction observed during ischemia/reperfasion by affecting endothelial cell survival. The effects of 8-iso-PGE2 and 8-iso-PGF2alpha, two abundantly produced isoprostanes, were studied on porcine endothelial cultures and isolated brain microvessels. Cell survival was evaluated by MTT reduction, double staining with DNA-binding fluorochromes and in situ DNA fragmentation labeling,
8-Iso-PGF2alpha (1--10 nM) induced 20--25% cell death in endothelial cultures after 24 h coincident with similar increase in the number of cells that become permeable to PI. On the contrary, 8-iso-PGE 2 did not affect endothelial cell survival. Approximately 9% of the cells suffered apoptosis. This percentage remained unchanged regardless the treatment. Several observations indicate a role for thromboxane A2 to mediate 8-iso-PGF2alpha-induced death: (1) the levels of thromboxane A2 increased dramatically in endothelial cultures after 8-iso-PGF2alpha-treatment; (2) inhibitors of thromboxane synthase, CGS12970 and U6355A and Ibuprofen, a non-selective inhibitor of cyclooxygenases, reverted the effect of the isoprostane; (3) analogs of thromboxane A2 U46619 and IBOP, reproduce the effect of 8-iso-PGF 2alpha after 24 h. 8-Iso-PGF2alpha also decreased endothelial viability on isolated brain microvessels. These results suggest, that 8-iso-PGF2alpha, might be a direct contributor to ischemia/reperfusion injury.
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Wateridge, David John. "Lymphocyte migration and the regulation of brain endothelial cell junctions." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446719/.

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Through bona fide tight junctions and regulated transcytosis, brain endothelial cells (ECs) are able to establish a blood-brain barrier (BBB) that regulates access of leucocytes and solutes to the central nervous systenn (CNS). Occludin was the first transmembrane tight junction protein identified and it has been demonstrated that expression of mutant occludin proteins in epithelial cells dramatically affects neutrophil transmigration and monolayer permeability. To determine if similar strategies could influence transendothelial lymphocyte migration and other endothelial barrier properties, a brain EC line (GPNT) was transfected with a range of occludin proteins and characterised by functional assays. Expression of wild-type occludin reduced T cell migration and, as in epithelial cells, this was shown to be dependent on an unmodified N-terminal domain. The mechanism(s) by which lymphocytes physically cross the endothelial barrier remains a poorly described stage of lymphocyte extravasation. The possibility remains, however, that modulation of endothelial cell-cell junctions is a necessary pre-requisite to physically allow the passage of a leucocyte through the EC wall, i.e the paracellular pathway. The firm adhesion of circulating T cells to BBB ECs is predominantly via ICAM- 1, a cell adhesion molecule of the immunoglobulin superfamily expressed on the EC and previously demonstrated to be capable of signal transduction. A hypothesis was generated that I CAM-1 engagement facilitates diapedesis by activating signalling pathways that regulate cell-cell junctions. Using GPNT EC, the role of ICAM-1 in regulating junctional proteins and integrity was assessed. Following crosslinking of ICAM-1, both VE-cadherin and PECAM showed increased tyrosine phosphorylation with identical experiments showing that ICAM-1 crosslinking correlated with an increase in transmonolayer permeability to molecular tracers. Immunoprecipitated VE-cadherin showed no change in its association with p- or y-catenin following ICAM-1 crosslinking, however, there was increased association of both catenins with PECAM via a rho-dependent/ROCK- independent pathway. The existence of such pathways suggests that pharmacological targeting of ICAM-1-mediated signalling may be advantageous in the therapeutic management of neuroinflammatory diseases.
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Vogt, Camille Janette. "Microvascular oxidative injury, endothelial cell death, and capillary rarefaction in glucocorticoid-induced hypertension /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9938582.

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Prat, Alexandre. "Human brain endothelial cells under inflammatory challenge : relevance to MS and T cell migration." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37815.

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Multiple sclerosis (MS) is considered an immune-mediated disorder of the central nervous system (CNS) characterized by multifocal areas of inflammation and demyelination. Lesion formation depends on migration of lymphocytes from the systemic compartment into the CNS through the blood-brain barrier. We have defined molecular and functional properties of human brain derived microvascular endothelial cells and of T lymphocytes that regulate the migration process and analysed how changes in these properties, in response to inflammatory conditions, contribute to the pathogenesis of multiple sclerosis. Rates of migration of T lymphocytes derived from patients with MS across either a fibronectin and/or endothelial cell barrier in vitro were increased compared to cells obtained from healthy controls. In the MS patients, migration rate correlated with disease activity, defined by clinical and MRI criteria and with IFN gamma production by T cells. Migration was reduced in patients receiving current therapies for MS. Adhesion molecules, chemokines and matrix metalloproteinases were all found to regulate the migration of MS derived lymphocytes through proteins of the basement membrane and human brain endothelial cells. We further demonstrated that the migratory properties of lymphocytes and both permeability and chemokine production by human brain endothelial cells, can be regulated via signalling through the specific kinin B1 receptor that is up-regulated on lymphocytes and human brain endothelial cells during inflammation, providing a potential novel therapeutic approach to modulate lymphocyte-endothelial cell interactions.
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Books on the topic "Brain capillary endothelial cell"

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Frithjof, Hammersen, Lewis David H, and World Congress for Microcirculation. (3rd : 1984 : Oxford, Oxfordshire), eds. Endothelial cell vesicles: Proceedings of a workshop at the Third World Congress for Microcirculation, Oxford/United Kingdom, September 9th-14th, 1984. Basel ; New York: Karger, 1985.

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Banjara, Manoj, and Damir Janigro. Effects of the Ketogenic Diet on the Blood-Brain Barrier. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0030.

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Ketone bodies (KBs) are always present in the blood, and their levels increase after high-fat diet intake, prolonged exercise, or extended fasting. Thus, one can predict effects on the brain capillary endothelium from high levels of ketones in the blood. Prolonged exposure of blood-brain barrier (BBB) endothelial cells to KBs induces expression of monocarboxylate transporters and enhances brain uptake of KBs. In addition, cell migration and expression of gap junction proteins are up-regulated by KBs. Thus, beneficial effects of the ketogenic diet may depend on increased brain uptake of KBs to match metabolic demand and repair of a disrupted BBB. As the effects of KBs on the BBB and their transport mechanisms across the BBB are better understood, it will be possible to develop alternative strategies to optimize the therapeutic benefits of KBs for brain disorders where the BBB is compromised.
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Sun, Lisa, and Michael V. Johnston. Rickettsial Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0157.

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Tick-borne rickettsioses are emerging as more important health problems throughout the world. The spotted fever group including Rickettsia rickettsia can cause encephalopathy, meningitis and brain damage by selectively targeting capillary endothelial cells in the brain, and stimulating inflammation, capillary leakage, hemorrhage, and intravascular coagulation. Rickettsia are are arthropod-borne gram-negative coccobacilli bacteria and are obligate intracellular organisms that do not survive in artificial medium. In North and South America, the most common rickettsial disorder is rocky mountain spotted fever (RMSF) transmitted by the dog tick Dermacentor variabilis or the wood tick Dermacentor andersoni. A characteristic “starry sky” pattern can be seen on MRI imaging of the brain in some patients with RMSF encephalopathy and is thought to reflect the organisms targeting of brain endothelial cells in capillaries the white matter. Early treatment with doxycycline is curative and reverses signs of encephalopathy if given within a few day of onset, but delayed treatment can be associated with permanent neurological disability. The typhus group of rickettsia bacteria include R. prowazekii, which causes epidemic typhus and R. typhi, which causes murine typhus (endemic) typhus in tropical and subtropical parts of the world. Flying squirrels and humans carry R prowazekii and rats are carry R. typhi. Q fever caused by the rickettsia organism Coxiella burnetti is transmitted from farm animals including sheep and is seen throughout the world including the United States.
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(Editor), David H. Lewis, ed. Endothelial Cell Vesicles (Progress in Applied Microcirculation, Vol 9). S. Karger AG (Switzerland), 1985.

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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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Book chapters on the topic "Brain capillary endothelial cell"

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Pardridge, William M. "Brain Capillary Endothelial Transport of Insulin." In Endothelial Cell Dysfunctions, 347–62. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-0721-9_21.

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Nagashima, Tatsuya, W. Shigin, A. Mizoguchi, M. Arakawa, M. Yamaguchi, and N. Tamaki. "The Effect of Leukotriene C4 on the Permeability of Brain Capillary Endothelial Cell Monolayer." In Brain Edema IX, 55–57. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_14.

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Kawai, N., R. M. McCarron, and Maria Spatz. "The Effect of Endothelins on Ion Transport Systems in Cultured Rat Brain Capillary Endothelial Cells." In Brain Edema X, 138–40. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_42.

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Dehouck, M. P., M. Chamoux, J. C. Fruchart, G. Spik, J. Montreuil, and R. Cecchelli. "Angiogenin Acts as a Direct Mitogen on Bovine Brain Capillary Endothelial Cells." In Vascular Endothelium, 249. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_29.

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Samoto, Ken, K. Ikezaki, N. Yokoyama, and M. Fukui. "P-Glycoprotein Expression in Brain Capillary Endothelial Cells After Focal Ischemia in Rat." In Brain Edema IX, 257–60. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_68.

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Wu, S., Tatsuya Nagashima, K. Ikeda, T. Kondoh, M. Yamaguchi, and N. Tamaki. "The Mechanism of Free Radical Generation in Brain Capillary Endothelial Cells After Anoxia and Reoxygenation." In Brain Edema X, 37–39. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_11.

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Ikeda, K., Tatsuya Nagashima, S. Wu, M. Yamaguchi, and N. Tamaki. "The Role of Calcium Ion in Anoxia/Reoxygenation Damage of Cultured Brain Capillary Endothelial Cells." In Brain Edema X, 4–7. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_2.

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Tewes, Bernhard J., and Hans-Joachim Galla. "Membrane Fractionation of Brain Capillary Endothelial Cells and Analysis of Lipid Polarity." In Biology and Physiology of the Blood-Brain Barrier, 97–101. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_17.

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Nagashima, Tatsuya, K. Ikeda, S. Wu, T. Kondo, M. Yamaguehi, and N. Tamaki. "The Mechanism of Reversible Osmotic Opening of the Blood-Brain Barrier: Role of Intracellular Calcium Ion in Capillary Endothelial Cells." In Brain Edema X, 231–33. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_71.

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Giese, H., K. Mertsch, R. F. Haselof, F. H. Härtel, and I. E. Blasig. "Hypoxia and Reoxygenation of a Cellular Barrier Consisting of Brain Capillary Endothelial Cells and Astrocytes." In Biology and Physiology of the Blood-Brain Barrier, 317–22. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_51.

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Conference papers on the topic "Brain capillary endothelial cell"

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Savion, N., A. Gamliel, and N. Farzame. "THROMBIN INTERACTION WITH CULTURED AORTIC AND CAPILLARY ENDOTHELIAL CELLS: BINDING, INTERNALIZATION, DEGRADATION AND RELEASE OF PROTEASE NEXINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644734.

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Thrombin (Th) binds specifically to confluent cultures of bovine aortic (ABAE) and brain capillary (BBC) endothelial cells. Saturation of 125I-Th binding is observed after 1 h exposure to the ligand and at an extracellular concentration of 0.5 and 1.0 µg/ml for ABAE and BBC cells, respectively. Under optimal conditions both ABAE and BBC cultures bind about 2 to 5 ng/106 cells, which represents about 20% of Th binding.to bovine corneal endothelial (BCE) cells. The cell associated 125I-Th in ABAE and BBC cells is internalized and degraded as described in BCE cells. The nature of the cell associated radioactivity is analyzed on SDS-polyacrylamide -gel electrophoresis and in ABAE and BBC cells about 30% of the I-Th appears in a complex with protease nexin I (PN I) while in BCE cells about 70% of the binding is mediated by PN I. ABAE cells possess 3 types of complexes, one which appears only on the cell surface with a molecular weight of 78 kDa, and two other complexes which appear only in the conditioned medium (CM) with molecular weights of 84 and 85 kDa. BBC and BCE cells demonstrate only one type of complex with a molecular weight of 77 kDa which appears both on the cell surface and in the CM. Preincubation of BCE cultures in the presence of Th is known to up-regulate the amount of PN I on the cell surface and in the CM, but this Th induced up-regulation effect is not observed in ABAE or BBC cells.The results described above indicate a difference between ABAE and BBC cells although both cell types growunder similar conditins and demonstrate similar morphological appearance. However, in both vascular endothelial cell types the total amount of PN I and its metabolism is relatively small compared to corneal endothelial cells. It, therefore, may indicate the lower capacity of vascular endothelial cells to control serine proteases activity at or near their cell surfaces as compared to corneal endothelial cells. This research was supported by a grant from the NationalCouncil for Research and Development, Israel and G.S.F. Munchen, Germany
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Fujimoto, T., B. Djuricic, K. Tanoue, Y. Fukushima, and H. Yamazaki. "CHANGES IN ENZYMATIC ACTIVITIES IN BRAIN CAPILLARY ENDOTHELIAL CELLS INJURED BY PLATELET AGGREGATION IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643368.

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We have reported cerebrovascular injuries induced by platelet aggregation in vivo. Appearance of vacuoles in endothelial cells and eventual deendothelialization are characteristic in large cerebral arteries (Stroke, 16:245, 1985). Minor changes are observed in brain capillaries, but disturbances of blood-brain barrier (BBB) are seen. To analyse changes in BBB, enzymatic activities in capillary endothelial cells before and after ADP-induced platelet aggregation in vivo were investigated.80 mg/kg of ADP was injected through a catheter into the right internal carotid artery of 32 rabbits. One hr later, right and left cortexes freed from pial membranes were homogenized and microvessels were isolated using discontinuous sucrose gradient ultracentrifugation. Purity of microvessel fraction was ascertained microscopically. The follwing enzymatic activities in these samples were measured.; cytochrome C oxydase (CCO), monoamine oxidase (MAO), p-nitrophenyl-phosphatase transferase (pNPPase, K-dependent component of Na, K-ATPase), gamma-glutamyl transferase (GT) and adenylate cyclase (AC). The enzymatic activities did not change after a vehicle-injection and did not show any differences between capillaries of both the cortexes before the ADP-injection. One hr after the ADP, GT and CCO activities decreased significantly in the capillaries of injection side. MAO activity also reduced without significance. The other enzymes did not show significant changes in their activities. Although pNPPase and AC which are associated with inner surface of plasma membrane were preserved well, activity of GT which is associated with outer portion of the membrane decreased significantly. It suggests superficial luminal injury and that plasma membrane might be affected from the side of vascular lumen. Reduced CCO activity suggests that disturbance in BBB is probably related to the increase in vesicular transportation and/or energy failure. Reduction of MAO activity indicates that damages to mitochondria exist in the capillaries. Cerebral blood vessels are prone to damage by released substances from activated platelet in vivo.
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Menasni, S., W. Hornebeck, L. Robert, and Y. Legrand. "ELASTASE TYPE ACTIVITY OF ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643360.

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Elastin degrading enzymes have been reported in the vessel wall and both fibroblasts and smooth muscle cells have been shown to produce elastase type enzymes in culture. Data is presented here showing that porcine aortic endothelial cells produce enzyme activities hydrolyzing elastin and synthetic substrates I Sue Ala Ala Ala nitroanilide, SAPNAI considered specific for elastase. Enzyme activity against the SAPNA but not against H-elastin was found to be associated with the cells after triton lysis .This activity was not secreted into the culture medium . The elastolytic activity has been partially characterized in relation to the kinetic of hydrolysis, pH optimum and susceptibility to different inhibitors. These studies revealed the presence of at least two enzymes: a metalo-protease with a pH optimum of 7.5 which accounts for approx. 80% of the total activity, and a serine protease with pH optimum of 8.0 which accounts for the remaining 20% . When the conditioned culture medium was studied, virtually no proteolytic activity could be detected even after activation with an organomercurial agent. However fractionation of the culture medium by gel filtration on HPLC resulted in elastolytic activity both against H-elastin and SAPNA. Proteolytic activity against casein could also be revealed after separation on SDS-PAGE. It is likely that these separation techniques remove an inhibitor also produced by the endothelial cells and allow the expression of proteolytic activity. That the elastolytic activity and the caseinolytic activity revealed by HPLC and PAGE respectively represent the activity of the same enzyme hase not yet been determined, and its relationship to the Stromelysin described by Herron et al(J. Biol. Chem. , 1986, 261. 2810-2813) in rabbit brain capillary endothelial cells is being investigated.
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Cambianica, I., M. Bossi, P. Gasco, W. Gonzalez, J. M. Idee, G. Miserocchi, R. Rigolio, et al. "Targeting Cells With MR Imaging Probes: Cellular Interaction And Intracellular Magnetic Iron Oxide Nanoparticles Uptake In Brain Capillary Endothelial and Choroidal Plexus Epithelial Cells." In BONSAI PROJECT SYMPOSIUM: BREAKTHROUGHS IN NANOPARTICLES FOR BIO-IMAGING. AIP, 2010. http://dx.doi.org/10.1063/1.3505065.

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Rodarte, Gabriela Pereira, Álvaro Maciel Campos Resende, Gabriel Paz Souza Mota, Larissa Julie Florindo, and Ana Laura Maciel Almeida. "Cognitive Symptoms in PostCovid-19 Patients: A Systematic Review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.500.

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Background: Although the main reported manifestation of COVID-19 is respiratory syndrome, several organs can be affected, including the central nervous system (CNS), which might cause cognitive changes. Objectives: Evaluate the relationship between COVID-19 and cognitive symptoms in infected patients with Sars-CoV-2. Methods: A search was performed using PubMed, Embase, BVS and Web of Science databases with the descriptors: “Cognitive symptoms”, “Brain fog”, “Covid-19” and “Sars-CoV-2”. The inclusion criteria were: articles in English and peer-reviewed; the exclusion criteria were: those who did not address cognitive symptoms after COVID- 19 and systematic reviews. Six articles were included. Results: Decline in memory and executive functions were the main reported cognitive symptoms. Greater susceptibility of the prefrontal cortex may explain neuropsychiatric morbidities, hence the increased risk of cognitive symptoms after acute infection. Sars-CoV-2 can trigger a high immune response that leads to the production of autoantibodies that can act against nervous tissue. Cortical hypometabolism, without direct cortical involvement and death of neurons, has been reported, which can be associated with damage to the white matter. Therefore, the deterioration could be reversible. Inflammation of endothelial cells and deposition of megakaryocytes can cause microvasculopathy and deposition of microcoagulants in capillary cortices. Cognitive deficits linked to the length of hospital stay have also been reported, especially in patients admitted to the ICU. Conclusions: There was a relationship between infection by Sars-CoV-2 and cognitive changes, mainly executive functions and working memory. Mechanisms might be related to inflammatory processes, immune response and length of stay in the ICU.
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Tien, Joe, John L. Tan, Celeste M. Nelson, and Christopher S. Chen. "Building Cellular Microenvironments to Control Capillary Endothelial Cell Proliferation, Death, and Differentiation." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23154.

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Abstract The dynamic binding interactions between cell surface receptors and local bioactive ligands serves as the principal mechanism by which cells survey their microenvironment and accordingly modulate their behaviors, such as proliferation, differentiation, migration, and suicide. Using conventional and non-conventional microfabrication approaches to engineer well-defined cellular microenvironments, we are examining how cells recognize and respond to adhesive interactions with the insoluble extracellular matrix (ECM). We will discuss our approaches to control the architecture and geometry of the adhesive interactions, as well as our resulting progress in identifying and elucidating the mechanisms by which cells sense the physical, chemical, and structural information carried within the ECM. By developing these approaches to engineering cell-surface interactions, we hope to improve the interconnect between artificial surfaces and living cells.
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de Agostini, A., J. Marcum, and R. Rosenberg. "THE BINDING OF ANTITHROMBIN TO CAPILLARY ENDOTHELIAL CELLS GROWN IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643343.

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Cloned endothelial cells from rat epididymal fat pads synthesize anticoagulantly active heparan sulfate proteoglycans containing the disaccharide, GlcA→ AMN-3,6-O-SO3, which is a marker for the antithrombin-binding domain of heparin. To demonstrate that antithrombin (AT) binds to cell surface heparan sulfate, a binding assay employing 125I-AT and cell monolayers has been developed. Post-confluent endothelial cells (7 days) were incubated with radiolabeled AT for 1 h at 4° and washed with PBS. Bound radioactivity was quantitated after solubilizing whole cells. Under these conditions, ∼1% (2174±50 cpm/5x104 cells) of the 125I-AT bound to the endothelial cell monolayer, whereas none of the radiolabeled protein bound to CHO cells or bovine smooth muscle cells. Utilization of unlabeled AT (1 μM) in experiments conducted as described above resulted in a reduction (73%) of the binding of the labeled species to endothelial cells. To assess whether heparan sulfate was responsible for AT binding, cell monolayers were incubated for 1 h at 37° with purified Flavobacterium heparinase (0.2 units). Over 90% of 125I-AT binding to these cellular elements was suppressed with the bacterial enzyme. Internalization of radiolabeled AT by endothelial cells was examined by incubating the protease inhibitor and cells at 4° and 37 . An initial rapid binding was observed at both temperatures. At 4° AT binding plateaued within 15 min, whereas at 37° binding did not plateau until 60 min and was 30% greater than that observed at 4. These data suggest that surface-associated AT can be internalized by endothelial cells. In addition, AT binding was shown to increase with the length of endothelial cell postconfluence, indicating an accumulation of heparan sulfate by these cells during quiescence. In conclusion, our studies support the hypothesis that the vascular endothelium is coated with heparan sulfate-bound AT, which is responsible for the antithrombotic properties of these natural surfaces.
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Shimizu, Ri-ichiro, Ryo Suzuki, and Nobuki Kudo. "Visualization of Endothelial Cell Damage Caused by Ultrasonically Induced Microbubble Oscillation Inside a Capillary Phantom." In 2020 IEEE International Ultrasonics Symposium (IUS). IEEE, 2020. http://dx.doi.org/10.1109/ius46767.2020.9251785.

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Singh, Seema, Michelle L. Varney, and Rakesh K. Singh. "Abstract 3486: CXCR1 and CXCR2 silencing alters endothelial cell proliferation, migration and capillary tube formation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3486.

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Rodemer, Claus, Jürgen Jenne, Marc Fatar, Michael G. Hennerici, and Stephen Meairs. "Ultrasound fails to induce proliferation of human brain and mouse endothelial cell lines." In 12TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND. AIP, 2012. http://dx.doi.org/10.1063/1.4769909.

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Reports on the topic "Brain capillary endothelial cell"

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Paul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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