Journal articles: '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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Vigne, Paul, and Christian Frelin. "Endothelins activate phospholipase A2 in brain capillary endothelial cells." Brain Research 651, no. 1-2 (July 1994): 342–44. http://dx.doi.org/10.1016/0006-8993(94)90716-1.

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Paris-Robidas, Sarah, Danny Brouard, Vincent Emond, Martin Parent, and Frédéric Calon. "Internalization of targeted quantum dots by brain capillary endothelial cells in vivo." Journal of Cerebral Blood Flow & Metabolism 36, no. 4 (October 6, 2015): 731–42. http://dx.doi.org/10.1177/0271678x15608201.

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Receptors located on brain capillary endothelial cells forming the blood–brain barrier are the target of most brain drug delivery approaches. Yet, direct subcellular evidence of vectorized transport of nanoformulations into the brain is lacking. To resolve this question, quantum dots were conjugated to monoclonal antibodies (Ri7) targeting the murine transferrin receptor. Specific transferrin receptor-mediated endocytosis of Ri7-quantum dots was first confirmed in N2A and bEnd5 cells. After intravenous injection in mice, Ri7-quantum dots exhibited a fourfold higher volume of distribution in brain tissues, compared to controls. Immunofluorescence analysis showed that Ri7-quantum dots were sequestered throughout the cerebral vasculature 30 min, 1 h, and 4 h post injection, with a decline of signal intensity after 24 h. Transmission electron microscopic studies confirmed that Ri7-quantum dots were massively internalized by brain capillary endothelial cells, averaging 37 ± 4 Ri7-quantum dots/cell 1 h after injection. Most quantum dots within brain capillary endothelial cells were observed in small vesicles (58%), with a smaller proportion detected in tubular structures or in multivesicular bodies. Parenchymal penetration of Ri7-quantum dots was extremely low and comparable to control IgG. Our results show that systemically administered Ri7-quantum dots complexes undergo extensive endocytosis by brain capillary endothelial cells and open the door for novel therapeutic approaches based on brain endothelial cell drug delivery.

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BEAULIEU, Édith, Michel DEMEULE, Lucian GHITESCU, and Richard BÉLIVEAU. "P-glycoprotein is strongly expressed in the luminal membranes of the endothelium of blood vessels in the brain." Biochemical Journal 326, no. 2 (September 1, 1997): 539–44. http://dx.doi.org/10.1042/bj3260539.

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Luminal membranes of the vascular endothelium were isolated from brain, heart and lungs by modification of their density. The presence of P-glycoprotein (P-gp) was detected by Western blotting in luminal membranes from the endothelium of the three tissues. Strong enrichment in brain capillary luminal membranes, compared with brain capillaries (17-fold) and whole membranes (400–500-fold), indicates that P-gp is mainly located on the luminal side of the brain endothelium. Western blotting was also performed with antibodies directed against GLUT1, glial fibrillary acidic protein, adaptin, IP3R-3, integrins αv and collagen IV as controls to determine whether the preparations were contaminated by other membranes. Strong enrichment of GLUT1 in brain capillary luminal membranes (9.9-fold) showed that the preparation consisted mainly of endothelial cell plasma membranes. Poor enrichment of glial fibrillary acidic protein (1.4-fold) and adaptin (2.4-fold) and a decreased level of IP3R-3, integrins αv and collagen IV excludes the possibility of major contamination by astrocytes or internal and anti-luminal membranes. High levels of P-gp in the luminal membranes of brain capillary endothelial cells suggests that it may play an important role in limiting the access of anti-cancer drugs to the brain.

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Chen, Y., R. M. McCarron, S. Golech, J. Bembry, B. Ford, F. A. Lenz, N. Azzam, and M. Spatz. "ET-1- and NO-mediated signal transduction pathway in human brain capillary endothelial cells." American Journal of Physiology-Cell Physiology 284, no. 2 (February 1, 2003): C243—C249. http://dx.doi.org/10.1152/ajpcell.00305.2002.

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Previous studies have demonstrated that functional interaction between endothelin (ET)-1 and nitric oxide (NO) involves changes in Ca2+mobilization and cytoskeleton in human brain microvascular endothelial cells. The focus of this investigation was to examine the possible existence of analogous interplay between these vasoactive substances and elucidate their signal transduction pathways in human brain capillary endothelial cells. The results indicate that ET-1-stimulated Ca2+mobilization in these cells is dose-dependently inhibited by NOR-1 (an NO donor). This inhibition was prevented by ODQ (an inhibitor of guanylyl cyclase) or Rp-8-CPT-cGMPS (an inhibitor of protein kinase G). Treatment of endothelial cells with 8-bromo-cGMP reduced ET-1-induced Ca2+mobilization in a manner similar to that observed with NOR-1 treatment. In addition, NOR-1 or cGMP reduced Ca2+mobilization induced by mastoparan (an activator of G protein), inositol 1,4,5-trisphosphate, or thapsigargin (an inhibitor of Ca2+-ATPase). Interestingly, alterations in endothelial cytoskeleton (actin and vimentin) were associated with these effects. The data indicate for the first time that the cGMP-dependent protein kinase colocalizes with actin. These changes were accompanied by altered levels of phosphorylated vasodilator-stimulated phosphoprotein, which were elevated in endothelial cells incubated with NOR-1 and significantly reduced by ODQ or Rp-8-CPT-cGMPS. The findings indicate a potential mechanism by which the functional interrelationship between ET-1 and NO plays a role in regulating capillary tone, microcirculation, and blood-brain barrier function.

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Nagashima, Tatsuya, Shijing Wu, Michio Yamaguchi, and Norihiko Tamaki. "Reoxygenation Injury of Human Brain Capillary Endothelial Cells." Cellular and Molecular Neurobiology 19, no. 1 (February 1999): 151–61. http://dx.doi.org/10.1023/a:1006980911551.

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Zhu, Jiangwen, Karin Motejlek, Denan Wang, Keling Zang, Andrea Schmidt, and Louis F. Reichardt. "β8 integrins are required for vascular morphogenesis in mouse embryos." Development 129, no. 12 (June 15, 2002): 2891–903. http://dx.doi.org/10.1242/dev.129.12.2891.

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In order to assess the in vivo function of integrins containing the β8 subunit, we have generated integrin β8-deficient mice. Ablation of β8 results in embryonic or perinatal lethality with profound defects in vascular development. Sixty-five percent of integrin β8-deficient embryos die at midgestation, with evidence of insufficient vascularization of the placenta and yolk sac. The remaining 35% die shortly after birth with extensive intracerebral hemorrhage. Examination of brain tissue from integrin β8-deficient embryos reveals abnormal vascular morphogenesis resulting in distended and leaky capillary vessels, as well as aberrant brain capillary patterning. In addition, endothelial cell hyperplasia is found in these mutant brains. Expression studies show that integrin β8 transcripts are localized in endodermal cells surrounding endothelium in the yolk sac and in periventricular cells of the neuroepithelium in the brain. We propose that integrin β8 is required for vascular morphogenesis by providing proper cues for capillary growth in both yolk sac and embryonic brain. This study thus identifies a molecule crucial for vascular patterning in embryonic yolk sac and brain.

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Wang, Kang, Haifeng Zhang, Yun He, Quan Jiang, Yoshiaki Tanaka, In-Hyun Park, Jordan S. Pober, Wang Min, and Huanjiao Jenny Zhou. "Mural Cell-Specific Deletion of Cerebral Cavernous Malformation 3 in the Brain Induces Cerebral Cavernous Malformations." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2171–86. http://dx.doi.org/10.1161/atvbaha.120.314586.

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Objective: Cerebral cavernous malformations (CCM), consisting of dilated capillary channels formed by a single layer of endothelial cells lacking surrounding mural cells. It is unclear why CCM lesions are primarily confined to brain vasculature, although the 3 CCM-associated genes ( CCM1 , CCM2 , and CCM3 ) are ubiquitously expressed in all tissues. We aimed to determine the role of CCM gene in brain mural cell in CCM pathogenesis. Approach and Results: SM22α -Cre was used to drive a specific deletion of Ccm3 in mural cells, including pericytes and smooth muscle cells (Ccm3smKO). Ccm3smKO mice developed CCM lesions in the brain with onset at neonatal stages. One-third of Ccm3smKO mice survived upto 6 weeks of age, exhibiting seizures, and severe brain hemorrhage. The early CCM lesions in Ccm3smKO neonates were loosely wrapped by mural cells, and adult Ccm3smKO mice had clustered and enlarged capillary channels (caverns) formed by a single layer of endothelium lacking mural cell coverage. Importantly, CCM lesions throughout the entire brain in Ccm3smKO mice, which more accurately mimicked human disease than the current endothelial cell-specific CCM3 deletion models. Mechanistically, CCM3 loss in brain pericytes dramatically increased paxillin stability and focal adhesion formation, enhancing ITG-β1 (integrin β1) activity and extracellular matrix adhesion but reducing cell migration and endothelial cell-pericyte associations. Moreover, CCM3-wild type, but not a paxillin-binding defective mutant, rescued the phenotypes in CCM3-deficient pericytes. Conclusions: Our data demonstrate for the first time that deletion of a CCM gene in the brain mural cell induces CCM pathogenesis.

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Souza, Mariana C., Tatiana A. Padua, and Maria G. Henriques. "Endothelial-Leukocyte Interaction in Severe Malaria: Beyond the Brain." Mediators of Inflammation 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/168937.

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Malaria is the most important parasitic disease worldwide, accounting for 1 million deaths each year. Severe malaria is a systemic illness characterized by dysfunction of brain tissue and of one or more peripheral organs as lungs and kidney. The most severe and most studied form of malaria is associated with cerebral complications due to capillary congestion and the adhesion of infected erythrocytes, platelets, and leukocytes to brain vasculature. Thus, leukocyte rolling and adhesion in the brain vascular bed during severe malaria is singular and distinct from other models of inflammation. The leukocyte/endothelium interaction and neutrophil accumulation are also observed in the lungs. However, lung interactions differ from brain interactions, likely due to differences in the blood-brain barrier and blood-air barrier tight junction composition of the brain and lung endothelium. Here, we review the importance of endothelial dysfunction and the mechanism of leukocyte/endothelium interaction during severe malaria. Furthermore, we hypothesize a possible use of adjunctive therapies to antimalarial drugs that target the interaction between the leukocytes and the endothelium.

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Robinson, DH, MK Warren, LT Liang, JJ Oprandy, TB Nielsen, and YH Kang. "Retroviral transformation of cerebral microvascular endothelial cells: macrophage-like and microvascular endothelial cell properties." Blood 77, no. 2 (January 15, 1991): 294–305. http://dx.doi.org/10.1182/blood.v77.2.294.bloodjournal772294.

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We report that L-cell-conditioned medium (LCM) transforms porcine cerebral microvascular (PCMV) endothelial cells into cells with macrophage-like properties. LCM is known to contain both cytokine(s) and the L-cell virus, a murine retrovirus found in the L929 cell and LCM. Our evidence suggests that both LCM cytokine(s) and the L-cell virus are involved in this PCMV endothelial cell transformation. Criteria for transformation include focus formation, decreased serum requirements for growth, changes in morphology including nonadherence, propagation in suspension culture, and a decreased growth response to stimulation with a known endothelial cell mitogen. Macrophage-like characteristics of this transformed cell, designated as RVTE, include pinocytosis of low-density lipoprotein, Fc receptor-mediated phagocytosis, phagocytosis of bacteria and zymosan, the expression of macrophage enzyme markers, and constitutive production of colony- stimulating factor 1. However, the transformed cell retains several properties of the nontransformed cell including the expression of FVIII:RAg and in vitro self-organization into capillary-like structures. Cloning of RVTE cells clearly shows that both macrophage- like and cerebral microvascular endothelial cell properties are present in the same cell. During self-organization, nontransformed cells express morphologic and functional characteristics classically associated with the macrophage. These findings suggest that some brain capillary pathophysiologies could involve macrophage-like cerebral microvascular endothelial cells. Furthermore, the “reticuloendothelial” phenotypic repertoire expressed by this transformed cerebral microvascular endothelial cell may show that the cerebral capillary endothelial cell in vivo is derived from a hematopoietic and/or phagocytic precursor.

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Tewes, B. J., and H. J. Galla. "Lipid Polarity in Brain Capillary Endothelial Cells." Endothelium 8, no. 3 (January 2001): 207–20. http://dx.doi.org/10.1080/10623320109051566.

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Praça, Catarina, Susana C. Rosa, Emmanuel Sevin, Romeo Cecchelli, Marie-Pierre Dehouck, and Lino S. Ferreira. "Derivation of Brain Capillary-like Endothelial Cells from Human Pluripotent Stem Cell-Derived Endothelial Progenitor Cells." Stem Cell Reports 13, no. 4 (October 2019): 599–611. http://dx.doi.org/10.1016/j.stemcr.2019.08.002.

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Robinson, DH, MK Warren, LT Liang, JJ Oprandy, TB Nielsen, and YH Kang. "Retroviral transformation of cerebral microvascular endothelial cells: macrophage-like and microvascular endothelial cell properties." Blood 77, no. 2 (January 15, 1991): 294–305. http://dx.doi.org/10.1182/blood.v77.2.294.294.

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Abstract We report that L-cell-conditioned medium (LCM) transforms porcine cerebral microvascular (PCMV) endothelial cells into cells with macrophage-like properties. LCM is known to contain both cytokine(s) and the L-cell virus, a murine retrovirus found in the L929 cell and LCM. Our evidence suggests that both LCM cytokine(s) and the L-cell virus are involved in this PCMV endothelial cell transformation. Criteria for transformation include focus formation, decreased serum requirements for growth, changes in morphology including nonadherence, propagation in suspension culture, and a decreased growth response to stimulation with a known endothelial cell mitogen. Macrophage-like characteristics of this transformed cell, designated as RVTE, include pinocytosis of low-density lipoprotein, Fc receptor-mediated phagocytosis, phagocytosis of bacteria and zymosan, the expression of macrophage enzyme markers, and constitutive production of colony- stimulating factor 1. However, the transformed cell retains several properties of the nontransformed cell including the expression of FVIII:RAg and in vitro self-organization into capillary-like structures. Cloning of RVTE cells clearly shows that both macrophage- like and cerebral microvascular endothelial cell properties are present in the same cell. During self-organization, nontransformed cells express morphologic and functional characteristics classically associated with the macrophage. These findings suggest that some brain capillary pathophysiologies could involve macrophage-like cerebral microvascular endothelial cells. Furthermore, the “reticuloendothelial” phenotypic repertoire expressed by this transformed cerebral microvascular endothelial cell may show that the cerebral capillary endothelial cell in vivo is derived from a hematopoietic and/or phagocytic precursor.

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Faille, Dorothée, Fatima El-Assaad, Marie-Christine Alessi, Thierry Fusai, Valéry Combes, and Georges Grau. "Platelet-endothelial cell interactions in cerebral malaria: The end of a cordial understanding." Thrombosis and Haemostasis 102, no. 12 (2009): 1093–102. http://dx.doi.org/10.1160/th09-05-0337.

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SummaryCerebral malaria is an acute encephalopathy evolving from an infection with Plasmodium falciparum which kills more than one million people each year. Brain tissues from patients who died with cerebral malaria revealed multifocal capillary obstruction by parasitised red blood cells, platelets, and leukocytes. Many studies are unified in their proposal of two major hypotheses consisting of cell adhesion to the brain endothelium and excessive immune stimulation resulting in further vascular inflammation, prothrombotic cell activation, mechanical obstruction of cerebral capillaries and, consequently, blood-brain barrier disruption. Platelets and endothelial cells communicate on multiple levels. Infection-induced changes in platelets and endothelial cells occur in cerebral malaria, resulting in their concomitant activation, increased interactions between these two cell types, and a secondary procoagulant or hypercoagulable state. Here we review evidence for these mechanisms and highlight the possible role of platelets as effectors of endothelial damage in cerebral malaria. A better understanding of the complex regulation of these various interactions between brain endothelial cells and platelets in the context of cerebral malaria may prove useful in the development of new approaches to the treatment of this disease.

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Veszelka, Szilvia, Mária Mészáros, Gergő Porkoláb, Ágnes Rusznyák, Katalin Szászné Réti-Nagy, Mária A. Deli, Miklós Vecsernyés, Ildikó Bácskay, Judit Váradi, and Ferenc Fenyvesi. "Effects of Hydroxypropyl-Beta-Cyclodextrin on Cultured Brain Endothelial Cells." Molecules 27, no. 22 (November 10, 2022): 7738. http://dx.doi.org/10.3390/molecules27227738.

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The application of 2-hydroxypropyl-beta-cyclodextrin (HPBCD) in the treatment of the rare cholesterol and lipid storage disorder Niemann–Pick disease type C opened new perspectives in the development of an efficient therapy. Even if the systemic administration of HPBCD was found to be effective, its low permeability across the blood–brain barrier (BBB) limited the positive neurological effects. Nevertheless, the cellular interactions of HPBCD with brain capillary endothelial cells have not been investigated in detail. In this study, the cytotoxicity, permeability, and cellular internalization of HPBCD on primary rat and immortalized human (hCMEC/D3) brain capillary endothelial cells were investigated. HPBCD shows no cytotoxicity on endothelial cells up to 100 µM, measured by impedance kinetics. Using a fluorescent derivative of HPBCD (FITC-HPBCD) the permeability measurements reveal that on an in vitro triple co-culture BBB model, FITC-HPBCD has low permeability, 0.50 × 10−6 cm/s, while on hCMEC/D3 cell layers, the permeability is higher, 1.86 × 10−5 cm/s. FITC-HPBCD enters brain capillary endothelial cells, is detected in cytoplasmic vesicles and rarely localized in lysosomes. The cellular internalization of HPBCD at the BBB can help to develop new strategies for improved HPBCD effects after systemic administration.

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Abbott, N. J., C. C. Hughes, P. A. Revest, and J. Greenwood. "Development and characterisation of a rat brain capillary endothelial culture: towards an in vitro blood-brain barrier." Journal of Cell Science 103, no. 1 (September 1, 1992): 23–37. http://dx.doi.org/10.1242/jcs.103.1.23.

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Primary culture of rat brain endothelial cells is described, based on the method of C. C. W. Hughes and P. L. Lantos. The cells have been characterised using morphological and immunocytochemical techniques, and systematic studies undertaken to determine the optimal culture medium and conditions required to grow the cells at high purity on a variety of substrata. The endothelial cells have a spindle-shaped morphology, and proliferate as plaques from small clusters of cells associated with capillary fragments in the starting material. Tight junction-like cell:cell appositions are seen at the electron-microscopic level. The cells show characteristic staining for antigens recognized by antibodies against von Willebrand factor (Factor VIII-related antigen), angiotensin-converting enzyme (ACE), the transferrin receptor (Ox-26), actin and vimentin. They also show binding of the lectin from Ulex europaeus (UEA I). Potential contaminating cells include smooth muscle, fibroblasts, pericytes and meningeal cells. Contaminants can be kept to < ca. 5% by careful removal of large vessels and meninges during dissection, by brief treatment with Ca(2+)- and Mg(2+)-free saline, by growth in medium supplemented with plasma-derived serum treated for removal of platelet-derived growth factor (PDGF), and by occasional use of medium in which D-valine is substituted for L-valine. Cells attach well to collagen-coated plastic, less well to glass. Cells can be grown on transparent collagen filters (ICN, Cellagen and Costar, Transwell-Col), and on microcarrier beads (Pharmacia, Cytodex-3). The culture has proved to be a useful preparation for studies of cellular physiology, pharmacology and biochemistry of the brain endothelium, and represents a first step in producing an in vitro model of the rat blood-brain barrier.

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Cura, Anthony J., and Anthony Carruthers. "AMP kinase regulation of sugar transport in brain capillary endothelial cells during acute metabolic stress." American Journal of Physiology-Cell Physiology 303, no. 8 (October 15, 2012): C806—C814. http://dx.doi.org/10.1152/ajpcell.00437.2011.

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AMP-dependent kinase (AMPK) and GLUT1-mediated sugar transport in blood-brain barrier endothelial cells are activated during acute cellular metabolic stress. Using murine brain microvasculature endothelium bEnd.3 cells, we show that AMPK phosphorylation and stimulation of 3- O-methylglucose transport by the AMPK agonist AICAR are inhibited in a dose-dependent manner by the AMPK antagonist Compound C. AMPK α1- or AMPK α2-knockdown by RNA interference or AMPK inhibition by Compound C reduces AMPK phosphorylation and 3- O-methylglucose transport stimulation induced by cellular glucose-depletion, by potassium cyanide (KCN), or by carbonyl cyanide- p-trifluoromethoxy-phenylhydrazone (FCCP). Cell surface biotinylation studies reveal that plasma membrane GLUT1 levels are increased two- to threefold by cellular glucose depletion, AICAR or KCN treatment, and that these increases are prevented by Compound C and by AMPK α1- or α2-knockdown. These results support the hypothesis that AMPK activation in blood-brain barrier-derived endothelial cells directs the trafficking of GLUT1 intracellular pools to the plasma membrane, thereby increasing endothelial sugar transport capacity.

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Gelfand, R. A., H. J. Frank, E. Levin, and A. Pedram. "Brain and atrial natriuretic peptides bind to common receptors in brain capillary endothelial cells." American Journal of Physiology-Endocrinology and Metabolism 261, no. 2 (August 1, 1991): E183—E189. http://dx.doi.org/10.1152/ajpendo.1991.261.2.e183.

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The recent discovery of brain natriuretic peptides (BNP) that stimulates natriuresis, diuresis, and vascular smooth muscle relaxation in a manner similar to that of atrial natriuretic peptide (ANP) suggests the possibility that these endocrine hormones function via some common mechanism. Indirect evidence from several laboratories suggests that BNP and ANP may bind to the same receptors. We examined whether ANP and BNP bind to a common set of receptors in cultured bovine brain capillary endothelial cells and in bovine aortic endothelial cells. Scatchard plot analysis of binding data shows a similar dissociation constant (KD) of approximately 0.3 nM and a maximal binding capacity (Bmax) of 50 fmol/mg protein for both natriuretic peptides in brain capillary cells and 0.6 nM and 80 fmol/mg protein, respectively, in the aortic endothelial cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the affinity cross-linked receptor-ligand complex shows a strongly labeled 65-kDa receptor and a 125-kDa band that is likely to be a receptor of the guanylate cyclase type. ANP and BNP cross compete equally for binding to the two receptors identified on the gels. ANP and BNP also stimulate guanosine 3', 5'-cyclic monophosphate production in these cells, consistent with the presence of a functional guanylate cyclase-linked B receptor. We conclude that ANP and BNP share common receptors in brain capillary and aortic endothelial cells.

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Zhao, Yinan, Yanguo Xin, Zhiyi He, and Wenyu Hu. "Function of Connexins in the Interaction between Glial and Vascular Cells in the Central Nervous System and Related Neurological Diseases." Neural Plasticity 2018 (June 10, 2018): 1–13. http://dx.doi.org/10.1155/2018/6323901.

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Neuronal signaling together with synapse activity in the central nervous system requires a precisely regulated microenvironment. Recently, the blood-brain barrier is considered as a “neuro-glia-vascular unit,” a structural and functional compound composed of capillary endothelial cells, glial cells, pericytes, and neurons, which plays a pivotal role in maintaining the balance of the microenvironment in and out of the brain. Tight junctions and adherens junctions, which function as barriers of the blood-brain barrier, are two well-known kinds in the endothelial cell junctions. In this review, we focus on the less-concerned contribution of gap junction proteins, connexins in blood-brain barrier integrity under physio-/pathology conditions. In the neuro-glia-vascular unit, connexins are expressed in the capillary endothelial cells and prominent in astrocyte endfeet around and associated with maturation and function of the blood-brain barrier through a unique signaling pathway and an interaction with tight junction proteins. Connexin hemichannels and connexin gap junction channels contribute to the physiological or pathological progress of the blood-brain barrier; in addition, the interaction with other cell-cell-adhesive proteins is also associated with the maintenance of the blood-brain barrier. Lastly, we explore the connexins and connexin channels involved in the blood-brain barrier in neurological diseases and any programme for drug discovery or delivery to target or avoid the blood-brain barrier.

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Chamoux, M., M. P. Dehouck, J. C. Fruchart, G. Spik, J. Montreuil, and R. Cecchelli. "Characterization of angiogenin receptors on bovine brain capillary endothelial cells." Biochemical and Biophysical Research Communications 176, no. 2 (April 1991): 833–39. http://dx.doi.org/10.1016/s0006-291x(05)80261-x.

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Vigne, Paul, Julien Desmarets, Denis Guedin, and Christian Frelin. "Properties of an Endothelin-3-Sensitive Eta-like Endothelin Receptor in Brain Capillary Endothelial Cells." Biochemical and Biophysical Research Communications 220, no. 3 (March 1996): 839–42. http://dx.doi.org/10.1006/bbrc.1996.0491.

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Ketabi-Kiyanvash, Nahal, Christel Herold-Mende, Farzaneh Kashfi, Sandra Caldeira, Massimo Tommasino, Walter E. Haefeli, and Johanna Weiss. "NKIM-6, a new immortalized human brain capillary endothelial cell line with conserved endothelial characteristics." Cell and Tissue Research 328, no. 1 (December 19, 2006): 19–29. http://dx.doi.org/10.1007/s00441-006-0348-4.

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Sakurai, Yu, Himeka Watanabe, Kazuma Nishio, Kohei Hashimoto, Atsuki Harada, Masaki Gomi, Masayoshi Suzuki, et al. "pH-Responsive Lipid Nanoparticles Achieve Efficient mRNA Transfection in Brain Capillary Endothelial Cells." Pharmaceutics 14, no. 8 (July 27, 2022): 1560. http://dx.doi.org/10.3390/pharmaceutics14081560.

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The blood–brain barrier (BBB), which is comprised of brain capillary endothelial cells, plays a pivotal role in the transport of drugs from the blood to the brain. Therefore, an analysis of proteins in the endothelial cells, such as transporters and tight junction proteins, which contribute to BBB function, is important for the development of therapeutics for the treatment of brain diseases. However, gene transfection into the vascular endothelial cells of the BBB is fraught with difficulties, even in vitro. We report herein on the development of lipid nanoparticles (LNPs), in which mRNA is encapsulated in a nano-sized capsule composed of a pH-activated and reductive environment-responsive lipid-like material (ssPalm). We evaluated the efficiency of mRNA delivery into non-polarized human brain capillary endothelial cells, hCMEC/D3 cells. The ssPalm LNPs permitted marker genes (GFP) to be transferred into nearly 100% of the cells, with low toxicity in higher concentration. A proteomic analysis indicated that the ssPalm-LNP had less effect on global cell signaling pathways than a Lipofectamine MessengerMAX/GFP-encoding mRNA complex (LFN), a commercially available transfection reagent, even at higher mRNA concentrations.

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Kawai, Nobutoshi, Richard M. McCarron, and Maria Spatz. "Endothelins stimulate sodium uptake into rat brain capillary endothelial cells through endothelin A-like receptors." Neuroscience Letters 190, no. 2 (May 1995): 85–88. http://dx.doi.org/10.1016/0304-3940(95)11507-s.

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Durieu-Trautmann, O., N. Foignant-Chaverot, J. Perdomo, P. Gounon, A. D. Strosberg, and P. O. Couraud. "Immortalization of brain capillary endothelial cells with maintenance of structural characteristics of the blood-brain barrier endothelium." In Vitro Cellular & Developmental Biology - Animal 27, no. 10 (October 1991): 771–78. http://dx.doi.org/10.1007/bf02631242.

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Descamps, L., M. P. Dehouck, G. Torpier, and R. Cecchelli. "Receptor-mediated transcytosis of transferrin through blood-brain barrier endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (April 1, 1996): H1149—H1158. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1149.

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A cell culture model of the blood-brain barrier consisting of a coculture of bovine brain capillary endothelial cells (BBCECs) and astrocytes has been used to examine the mechanism of iron transport to the brain. Binding experiments showed that BBCECs express 35,000 high-affinity (concn at 50% receptor saturation = 11.3 +/- 2.1 nM) transferin (Tf) receptors per cell. In contrast to apo-transferrin (apoTf) we observed a specific transport of holo-transferrin (holoTf) across BBCECs. This transport was inhibited completely at low temperature. Moreover, the anti-Tf receptor antibody (OX-26) competitively inhibited holoTf uptake by BBCECs. Pulse-chase experiments demonstrated that only 10% of Tf was recycled to the luminal side of the cells, whereas the majority of Tf was transcytosed to the abluminal side; double-labeling experiments clearly demonstrated that iron crosses BBCECs bound to Tf. No intraendothelial degradation of Tf was observed, suggesting that the intraendothelial pathway through BBCECs bypasses the lysosomal compartment. These results clearly show that the iron-Tf complex is transcytosed across brain capillary endothelial cells by a receptor-mediated pathway without any degradation.

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Harraz, Osama F., Thomas A. Longden, Fabrice Dabertrand, David Hill-Eubanks, and Mark T. Nelson. "Endothelial GqPCR activity controls capillary electrical signaling and brain blood flow through PIP2 depletion." Proceedings of the National Academy of Sciences 115, no. 15 (March 26, 2018): E3569—E3577. http://dx.doi.org/10.1073/pnas.1800201115.

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Brain capillaries play a critical role in sensing neural activity and translating it into dynamic changes in cerebral blood flow to serve the metabolic needs of the brain. The molecular cornerstone of this mechanism is the capillary endothelial cell inward rectifier K+ (Kir2.1) channel, which is activated by neuronal activity–dependent increases in external K+ concentration, producing a propagating hyperpolarizing electrical signal that dilates upstream arterioles. Here, we identify a key regulator of this process, demonstrating that phosphatidylinositol 4,5-bisphosphate (PIP2) is an intrinsic modulator of capillary Kir2.1-mediated signaling. We further show that PIP2 depletion through activation of Gq protein-coupled receptors (GqPCRs) cripples capillary-to-arteriole signal transduction in vitro and in vivo, highlighting the potential regulatory linkage between GqPCR-dependent and electrical neurovascular-coupling mechanisms. These results collectively show that PIP2 sets the gain of capillary-initiated electrical signaling by modulating Kir2.1 channels. Endothelial PIP2 levels would therefore shape the extent of retrograde signaling and modulate cerebral blood flow.

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Vigne, Paul, Jean Philippe Breittmayer, and Christian Frelin. "Sensitization by calyculin A of brain capillary endothelial cells to endothelin-1." British Journal of Pharmacology 114, no. 5 (March 1995): 1014–16. http://dx.doi.org/10.1111/j.1476-5381.1995.tb13306.x.

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Moses, Ashlee V., and Jay A. Nelson. "HIV infection of human brain capillary endothelial cell — Implications for AIDS dementia." Advances in Neuroimmunology 4, no. 3 (January 1994): 239–47. http://dx.doi.org/10.1016/s0960-5428(06)80262-7.

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Fasler-Kan, Elizaveta, Claudia Suenderhauf, Natasha Barteneva, Birk Poller, Daniel Gygax, and Jörg Huwyler. "Cytokine signaling in the human brain capillary endothelial cell line hCMEC/D3." Brain Research 1354 (October 2010): 15–22. http://dx.doi.org/10.1016/j.brainres.2010.07.077.

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40

Kawai, Nobutoshi, Toshifumi Yamamoto, Hideko Yamamoto, Richard M. McCarron, and Maria Spatz. "Functional characterization of endothelin receptors on cultured brain capillary endothelial cells of the rat." Neurochemistry International 31, no. 4 (October 1997): 597–605. http://dx.doi.org/10.1016/s0197-0186(97)00018-1.

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41

Zorenko, Yevgeniya, Galina Gubina-Vakulyck, Olena Pavlova, Tatyana Gorbach, Elena Shchegelskaya, and Elena Omelchenko. "Dynamics of indicators of the endothelium morphofunctional state of the brain microcirculatory bed vessels in rats with nitrite-induced Alzheimer's type dementia on the background of mesenchymal stem cell administration." Medicinski casopis 55, no. 1 (2021): 18–26. http://dx.doi.org/10.5937/mckg55-31775.

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Objective. The aim of this study was to assess the vascular endothelium morphofunctional state of the brain microcirculatory bed in rats with nitrite-induced Alzheimer's type dementia on the background of stem cells administration. Methods. 14 days after the experiment's end, the endothelin-1, VEGF-A, eNOS, von Willebrand factor were determined in blood serum by the enzyme immunoassay and photometric methods in rats with a model of nitrite-induced dementia (14 and 28 days of sodium nitrite intraperitoneal introduction) with and without mesenchymal stem cells (MSCs) administration. The brain slices were stained according to the Einarson's method and immunohistochemically by staging the reaction with antibodies to VEGF. Results. With an increase in the sodium nitrite administration period, the degree of damage of brain capillaries and neurons increased, dystrophy of "surviving" neurons developed and ability to produce VEGF decreased. After 14 days of "regeneration period" in groups without MSCs administration, further stimulation of VEGF production by endotheliocytes, cortex and hippocampus neurons of varying degrees was observed. In groups where stem cells were introduced, the number of capillaries increased, with endothelial hyperplasia in some cases. Conclusion. In animals with nitrite-induced dementia, dose-dependent damage to the endothelium of the capillary bed is noted. From the first day damage the vascular regeneration can be proved by VEGF expression. The stem cells administration more effectively stimulates capillary regeneration, as evidenced by a noticeable increase of the number of brain capillaries.

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DEVRIES, H., A. MOOR, M. BLOMROOSEMALEN, A. DEBOER, D. BREIMER, T. VANBERKEL, and J. KUIPER. "Lymphocyte adhesion to brain capillary endothelial cells in vitro." Journal of Neuroimmunology 52, no. 1 (June 1994): 1–8. http://dx.doi.org/10.1016/0165-5728(94)90155-4.

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Yamaji, Ryoichi, Tadayuki Okada, Maki Moriya, Mikihiko Naito, Takashi Tsuruo, Kazutaka Miyatake, and Yoshihisa Nakano. "Brain Capillary Endothelial Cells Express two forms of Erythropoietin Receptor mRNA." European Journal of Biochemistry 239, no. 2 (July 15, 1996): 494–500. http://dx.doi.org/10.1111/j.1432-1033.1996.0494u.x.

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Michel, Uwe, Rita Zobotke, Michael Mäder, and Roland Nau. "Regulation of Matrix Metalloproteinase Expression in Endothelial Cells by Heat-Inactivated Streptococcus pneumoniae." Infection and Immunity 69, no. 3 (March 1, 2001): 1914–16. http://dx.doi.org/10.1128/iai.69.3.1914-1916.2001.

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ABSTRACT Matrix metalloproteinases (MMPs) may contribute to an impaired endothelial layer in several diseases. We examined the effect of heat-inactivated Streptococcus pneumoniae R6 on MMP-2 and MMP-9 release by cultured aortic and brain capillary endothelial cells. Treatment with heat-inactivated S. pneumoniae caused an increased release of MMP-2 by both cell types.

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Romero, Ignacio A., Marie-Christine Prevost, Emmanuelle Perret, Peter Adamson, John Greenwood, Pierre-Olivier Couraud, and Simona Ozden. "Interactions between Brain Endothelial Cells and Human T-Cell Leukemia Virus Type 1-Infected Lymphocytes: Mechanisms of Viral Entry into the Central Nervous System." Journal of Virology 74, no. 13 (July 1, 2000): 6021–30. http://dx.doi.org/10.1128/jvi.74.13.6021-6030.2000.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) is associated with a variety of clinical manifestations, including tropical spastic paraparesis or HTLV-1-associated myelopathy (TSP/HAM). Viral detection in the central nervous system (CNS) of TSP/HAM patients demonstrates the ability of HTLV-1 to cross the blood-brain barrier (BBB). To investigate viral entry into the CNS, rat brain capillary endothelial cells were exposed to human lymphocytes chronically infected by HTLV-1 (MT2), to lymphocytes isolated from a seropositive patient, or to a control lymphoblastoid cell line (CEM). An enhanced adhesion to and migration through brain endothelial cells in vitro was observed with HTLV-1-infected lymphocytes. HTLV-1-infected lymphocytes also induced a twofold increase in the paracellular permeability of the endothelial monolayer. These effects were associated with an increased production of tumor necrosis factor alpha by HTLV-1-infected lymphocytes in the presence of brain endothelial cells. Ultrastructural analysis showed that contact between endothelial cells and HTLV-1-infected lymphocytes resulted in a massive and rapid budding of virions from lymphocytes, followed by their internalization into vesicles by brain endothelial cells and apparent release onto the basolateral side, suggesting that viral particles may cross the BBB using the transcytotic pathway. Our study also demonstrates that cell-cell fusion occurs between HTLV-1-infected lymphocytes and brain endothelial cells, with the latter being susceptible to transient HTLV-1 infection. These aspects may help us to understand the pathogenic mechanisms associated with neurological diseases induced by HTLV-1 infection.

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Itoh, Yoshiaki, and Norihiro Suzuki. "Control of Brain Capillary Blood Flow." Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (February 1, 2012): 1167–76. http://dx.doi.org/10.1038/jcbfm.2012.5.

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While it has been widely confirmed that cerebral blood flow is closely coupled with brain metabolism, it remains a matter of controversy whether capillary flow is directly controlled to meet the energy demands of the parenchyma. Since the capillary is known to lack smooth muscle cells, it has generally been considered that capillary flow is not regulated in situ. However, we now have increasing data supporting the physiological control of capillary flow. The observation of heterogeneity in the microcirculation in vivo has suggested that intravascular factors may be involved in the flow control, including non-Newtonian rheology, red blood cell flow, leukocyte adhesion, release of vasoactive mediators, and expression of glycoproteins on the endothelial cells. Astrocytes, a key mediator of the neurovascular unit, and intrinsic innervation may also regulate capillary flow. In addition, recent findings on pericyte contractility have attracted the attention of many researchers. Finally, based on these findings, we present a new model of flow control, the proximal integration model, in which localized neural activity is detected at nearby capillaries and the vasodilation signal is transmitted proximally along the vessel. Signals are then integrated at the precapillary arterioles and other arterioles further upstream and regulate the capillary flow.

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Meyer, Jörg, Uwe Mischeck, Maike Veyhl, Karin Henzel, and Hans-Joachim Galla. "Blood-brain barrier characteristic enzymatic properties in cultured brain capillary endothelial cells." Brain Research 514, no. 2 (April 1990): 305–9. http://dx.doi.org/10.1016/0006-8993(90)91425-g.

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Huang, Rong-qin, Wei-lun Ke, Ying-hua Qu, Jian-hua Zhu, Yuan-ying Pei, and Chen Jiang. "Characterization of lactoferrin receptor in brain endothelial capillary cells and mouse brain." Journal of Biomedical Science 14, no. 1 (October 18, 2006): 121–28. http://dx.doi.org/10.1007/s11373-006-9121-7.

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Sovic, Andrea, Ute Panzenboeck, Andrea Wintersperger, Ingrid Kratzer, Astrid Hammer, Sanja Levak-Frank, Sasa Frank, Daniel J. Rader, Ernst Malle, and Wolfgang Sattler. "Regulated expression of endothelial lipase by porcine brain capillary endothelial cells constituting the blood-brain barrier." Journal of Neurochemistry 94, no. 1 (July 2005): 109–19. http://dx.doi.org/10.1111/j.1471-4159.2005.03175.x.

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Roitbak, Tamara, Lu Li, and Lee Anna Cunningham. "Neural Stem/Progenitor Cells Promote Endothelial Cell Morphogenesis and Protect Endothelial Cells against Ischemia via HIF-1α-Regulated VEGF Signaling." Journal of Cerebral Blood Flow & Metabolism 28, no. 9 (May 14, 2008): 1530–42. http://dx.doi.org/10.1038/jcbfm.2008.38.

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Vascular cells provide a neural stem/progenitor cell (NSPC) niche that regulates expansion and differentiation of NSPCs within the germinal zones of the embryonic and adult brain under both physiologic and pathologic conditions. Here, we examined the NSPC—endothelial cell (NSPC/EC) interaction under conditions of ischemia, both in vitro and after intracerebral transplantation. In culture, embryonic mouse NSPCs supported capillary morphogenesis and protected ECs from cell death induced by serum starvation or by transient oxygen and glucose deprivation (OGD). Neural stem/progenitor cells constitutively expressed hypoxia-inducible factor 1α (HIF-1α) transcription factor and vascular endothelial growth factor (VEGF), both of which were increased approximately twofold after the exposure of NSPCs to OGD. The protective effects of NSPCs on ECs under conditions of serum starvation and hypoxia were blocked by pharmacological inhibitors of VEGF signaling, SU1498 and Flt-1-Fc. After intracerebral transplantation, NSPCs continued to express HIF-1α and VEGF, and promoted microvascular density after focal ischemia. These studies support a role for NSPCs in stabilization of vasculature during ischemia, mediated via HIF-1α-VEGF signaling pathways, and suggest therapeutic application of NSPCs to promote revascularization and repair after brain injury.

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Journal articles on the topic 'Brain capillary endothelial cell'

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