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Journal articles on the topic 'Brain microvascular endothelium'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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1

Avsenik, Jernej, Sotirios Bisdas, and Katarina Surlan Popovic. "Blood-brain barrier permeability imaging using perfusion computed tomography." Radiology and Oncology 49, no. 2 (2015): 107–14. http://dx.doi.org/10.2478/raon-2014-0029.

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Abstract Background. The blood-brain barrier represents the selective diffusion barrier at the level of the cerebral microvascular endothelium. Other functions of blood-brain barrier include transport, signaling and osmoregulation. Endothelial cells interact with surrounding astrocytes, pericytes and neurons. These interactions are crucial to the development, structural integrity and function of the cerebral microvascular endothelium. Dysfunctional blood-brain barrier has been associated with pathologies such as acute stroke, tumors, inflammatory and neurodegenerative diseases. Conclusions. Bl

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Rochfort, Keith D., Laura E. Collins, Alisha McLoughlin, and Philip M. Cummins. "Shear-Dependent Attenuation of Cellular ROS Levels can Suppress Proinflammatory Cytokine Injury to Human Brain Microvascular Endothelial Barrier Properties." Journal of Cerebral Blood Flow & Metabolism 35, no. 10 (2015): 1648–56. http://dx.doi.org/10.1038/jcbfm.2015.102.

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The regulatory interplay between laminar shear stress and proinflammatory cytokines during homeostatic maintenance of the brain microvascular endothelium is largely undefined. We hypothesized that laminar shear could counteract the injurious actions of proinflammatory cytokines on human brain microvascular endothelial cell (HBMvEC) barrier properties, in-part through suppression of cellular redox signaling. For these investigations, HBMvECs were exposed to either shear stress (8 dynes/cm2, 24 hours) or cytokines (tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6), 0 to 100 ng/mL, 6 or 18

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Iovino, Federico, Grietje Molema, and Jetta J. E. Bijlsma. "Platelet Endothelial Cell Adhesion Molecule-1, a Putative Receptor for the Adhesion of Streptococcus pneumoniae to the Vascular Endothelium of the Blood-Brain Barrier." Infection and Immunity 82, no. 9 (2014): 3555–66. http://dx.doi.org/10.1128/iai.00046-14.

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ABSTRACTThe Gram-positive bacteriumStreptococcus pneumoniaeis the main causative agent of bacterial meningitis.S. pneumoniaeis thought to invade the central nervous system via the bloodstream by crossing the vascular endothelium of the blood-brain barrier. The exact mechanism by which pneumococci cross endothelial cell barriers before meningitis develops is unknown. Here, we investigated the role of PECAM-1/CD31, one of the major endothelial cell adhesion molecules, inS. pneumoniaeadhesion to vascular endothelium of the blood-brain barrier. Mice were intravenously infected with pneumococci and

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Satoh, Kei, Hidemi Yoshida, Tada-Atsu Imalzumi, Masayuki Koyama, and Shigeru Takamatsu. "Production of Platelet-Activating Factor by Porcine Brain Microvascular Endothelial Cells in Culture." Thrombosis and Haemostasis 74, no. 05 (1995): 1335–39. http://dx.doi.org/10.1055/s-0038-1649936.

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SummaryEndothelial cells produce platelet-activating factor (PAF), which is the key process in the interactions between the vascular wall and blood cells. To examine the production of PAF in brain microvasculature we have cultured brain endothelial cells and performed a comparative study with aortic endothelial cells. Fresh porcine brain was homogenized, and microvascular endothelial cells were separated by enzyme digestion. The cells were cultured in medium containing epidermal growth factor and bovine brain extract. Endothelial cells from the aorta of the same animal were cultured in a simil

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Janigro, D., G. A. West, E. L. Gordon, and H. R. Winn. "ATP-sensitive K+ channels in rat aorta and brain microvascular endothelial cells." American Journal of Physiology-Cell Physiology 265, no. 3 (1993): C812—C821. http://dx.doi.org/10.1152/ajpcell.1993.265.3.c812.

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The endothelium plays an important role in the modulation of vascular tone and blood cell activation. Extensive work has demonstrated that the release of endothelium-derived relaxing factor (EDRF) from the endothelium is evoked by a number of physical and chemical stimuli requiring Ca2+. Because endothelial cells do not express voltage-dependent Ca2+ channels, Ca2+ influxes following receptor activation may be facilitated by cell hyperpolarizations mediated by the activation of K+ conductances. There has been recent interest in the role of ATP-sensitive K+ channels (KATP) suggesting that KATP

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Chen, Ye, Richard M. McCarron, Joliet Bembry, et al. "Nitric Oxide Modulates Endothelin 1-Induced Ca2+ Mobilization and Cytoskeletal F-Actin Filaments in Human Cerebromicrovascular Endothelial Cells." Journal of Cerebral Blood Flow & Metabolism 19, no. 2 (1999): 133–38. http://dx.doi.org/10.1097/00004647-199902000-00003.

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A functional interrelation between nitric oxide (NO), the endothelial-derived vasodilating factor, and endothelin 1 (ET-1), the potent vasoconstrictive peptide, was investigated in microvascular endothelium of human brain. Nor-1 dose-dependently decreased the ET-1–stimulated mobilization of Ca2+. This response was mimicked with cGMP and abrogated by inhibitors of guanylyl cyclase or cGMP-dependent protein kinase G. These findings indicate that NO and ET-1 interactions involved in modulation of intracellular Ca2+ are mediated by cGMP/protein kinase G. In addition, Nor-1–mediated effects were as

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Garcia-Polite, Fernando, Jordi Martorell, Paula Del Rey-Puech, et al. "Pulsatility and high shear stress deteriorate barrier phenotype in brain microvascular endothelium." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (2016): 2614–25. http://dx.doi.org/10.1177/0271678x16672482.

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Microvascular endothelial cells at the blood–brain barrier exhibit a protective phenotype, which is highly induced by biochemical and biomechanical stimuli. Amongst them, shear stress enhances junctional tightness and limits transport at capillary-like levels. Abnormal flow patterns can reduce functional features of macrovascular endothelium. We now examine if this is true in brain microvascular endothelial cells. We suggest in this paper a complex response of endothelial cells to aberrant forces under different flow domains. Human brain microvascular endothelial cells were exposed to physiolo

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Sahagun, G., S. A. Moore, and M. N. Hart. "Permeability of neutral vs. anionic dextrans in cultured brain microvascular endothelium." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 1 (1990): H162—H166. http://dx.doi.org/10.1152/ajpheart.1990.259.1.h162.

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The luminal surface of vascular endothelium contains glycocalyx residues that establish an overall negative charge. Recent evidence has suggested that local endothelial surface charge properties may account for the permeability properties of various macromolecules. It has also been suggested that altered membrane charge on the luminal side may play a role in thrombogenesis and atherogenesis. The relationship of macromolecule charge to endothelial cell permeability was examined in vitro using mouse brain microvessel endothelial cells grown to confluence on a nitrocellulose filter separating a d

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Kaiser, Mathias, Malgorzata Burek, Stefan Britz, et al. "The Influence of Capsaicin on the Integrity of Microvascular Endothelial Cell Monolayers." International Journal of Molecular Sciences 20, no. 1 (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 c

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Nottet, H. S., Y. Persidsky, V. G. Sasseville, et al. "Mechanisms for the transendothelial migration of HIV-1-infected monocytes into brain." Journal of Immunology 156, no. 3 (1996): 1284–95. http://dx.doi.org/10.4049/jimmunol.156.3.1284.

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Abstract HIV-1 penetration of the brain is a pivotal event in the neuropathogenesis of AIDS-associated dementia. The establishment of productive viral replication or up-regulation of adhesion molecule expression on brain microvascular endothelial cells (BMVEC) could permit entry of HIV into the central nervous system. To investigate the contribution of both, we inoculated primary human BMVEC with high titer macrophage-tropic HIV-1 or cocultured them with virus-infected monocytes. In both instances, BMVEC failed to demonstrate productive viral replication. Cell to cell contact between monocytes

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Lecointre, Maryline, Michelle Hauchecorne, Armelle Chaussivert, et al. "The Efficiency of Glutamate Uptake Differs between Neonatal and Adult Cortical Microvascular Endothelial Cells." Journal of Cerebral Blood Flow & Metabolism 34, no. 5 (2014): 764–67. http://dx.doi.org/10.1038/jcbfm.2014.30.

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Glutamate transporters (excitatory amino-acid transporters (EAATs)) are essential for brain homeostasis. While previous studies indicate that the vascular endothelium contributes to glutamate efflux in the adult brain, little information is available regarding glutamate uptake in the immature brain. The present study shows a differential expression pattern of EAATs between cortical microvessels in adults and newborns. In addition, adult cortical endothelial cells take up glutamate more efficiently than neonatal cells. Our findings indicate age-specific changes in extracellular glutamate regula

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Barabutis, Nektarios. "Insights on supporting the aging brain microvascular endothelium." Aging Brain 1 (2021): 100009. http://dx.doi.org/10.1016/j.nbas.2021.100009.

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Hsu, P., M. Shibata, and C. W. Leffler. "Prostanoid synthesis in response to high CO2 in newborn pig brain microvascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (1993): H1485—H1492. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1485.

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Hypercapnia-induced cerebral vasodilation involves prostanoids in newborn pigs. However, the source of prostanoids has not been determined. The current study was designed to address the hypothesis that piglet cerebral microvascular endothelial cells increase their synthesis of prostanoids in response to high CO2. Microvascular endothelial cells, smooth muscle cells, and glia were isolated and grown in primary culture. They were identified morphologically and by indirect immunofluorescence staining. Cerebral microvascular endothelial cell cultures from newborn pigs produced equal amounts of 6-k

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Shusta, Eric V., Ruben J. Boado, Gary W. Mathern, and William M. Pardridge. "Vascular Genomics of the Human Brain." Journal of Cerebral Blood Flow & Metabolism 22, no. 3 (2002): 245–52. http://dx.doi.org/10.1097/00004647-200203000-00001.

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The microvasculature of the human brain plays an important role in the development and maintenance of the central nervous system and in the pathogenesis of brain diseases, and is the site of differential gene expression within the brain. However, human brain microvascular-specific genes may not be detected in whole-brain gene microarray because the volume of the brain microvascular endothelium is relatively small (0.1%) compared with the whole brain. Therefore, the differential gene expression within the human brain microvasculature was evaluated using suppression subtractive hybridization wit

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Schnitzer, J. E. "gp60 is an albumin-binding glycoprotein expressed by continuous endothelium involved in albumin transcytosis." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 1 (1992): H246—H254. http://dx.doi.org/10.1152/ajpheart.1992.262.1.h246.

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Albumin reduces capillary permeability and acts as a carrier for various small molecules. Recently, we identified a 60-kDa sialoglycoprotein (gp60) on the surface of cultured rat microvascular endothelial cells (MEC) that binds albumin and antiglycophorin serum (alpha-gp). We verified that alpha-gp recognizes the albumin-binding gp60 by affinity, purifying proteins from MEC extracts using immobilized albumin. gp60 was immunoblotted with alpha-gp only when the MEC extract was reacted with albumin and not in controls. We immunoprecipitated gp60 from biosynthetically radiolabeled MEC lysates and

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Janigro, D., T. S. Nguyen, E. L. Gordon, and H. R. Winn. "Physiological properties of ATP-activated cation channels in rat brain microvascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 4 (1996): H1423—H1434. http://dx.doi.org/10.1152/ajpheart.1996.270.4.h1423.

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Endothelial cells mediate the actions of a variety of vasoactive substances, including ATP. ATP vasodilatatory actions have been shown to depend on a calcium-dependent release of endothelium-derived relaxing factor(s) (EDRF). ATP induced a vasodilatation of pial penetrating microvessels when applied intraluminally; these relaxations were mediated by the endothelium and followed release of nitric oxide (NO), since they were sensitive to blockade of NO-synthesizing enzymes by NG-nitro-L-arginine (1 mM) and NG-mono-methyl-L-arginine (0.1 mM). We have also investigated the electrophysiological act

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Wu, Limin, Mohammad R. Islam, Janice Lee, et al. "ErbB3 is a critical regulator of cytoskeletal dynamics in brain microvascular endothelial cells: Implications for vascular remodeling and blood brain barrier modulation." Journal of Cerebral Blood Flow & Metabolism 41, no. 9 (2021): 2242–55. http://dx.doi.org/10.1177/0271678x20984976.

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Neuregulin (NRG)1 - ErbB receptor signaling has been shown to play an important role in the biological function of peripheral microvascular endothelial cells. However, little is known about how NRG1/ErbB signaling impacts brain endothelial function and blood-brain barrier (BBB) properties. NRG1/ErbB pathways are affected by brain injury; when brain trauma was induced in mice in a controlled cortical impact model, endothelial ErbB3 gene expression was reduced to a greater extent than that of other NRG1 receptors. This finding suggests that ErbB3-mediated processes may be significantly compromis

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Engelhardt, Britta. "β1-Integrin/Matrix Interactions Support Blood–Brain Barrier Integrity". Journal of Cerebral Blood Flow & Metabolism 31, № 10 (2011): 1969–71. http://dx.doi.org/10.1038/jcbfm.2011.98.

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Brain microvascular endothelium forms an active permeability barrier, the blood–brain barrier (BBB). In neurologic disorders, barrier properties of the BBB are often lost indicating their dependance on molecular cues of the brain microenvironment. In this issue, Osada et al demonstrate that the endothelial extracellular matrix (ECM) provides one of these cues. Their study shows that β1-integrin-mediated adhesion of brain endothelial cells to the surrounding ECM is critical for stabilizing claudin-5 in BBB tight junctions (TJs) and BBB integrity. These observations point to a novel intracellula

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Thakar, Manjusha, Midrelle E. Noumbissi, and Monique F. Stins. "Microvascular Environment Influences Brain Microvascular Heterogeneity: Relative Roles of Astrocytes and Oligodendrocytes for the EPCR Expression in the Brain Endothelium." International Journal of Molecular Sciences 24, no. 8 (2023): 6908. http://dx.doi.org/10.3390/ijms24086908.

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Postmortem neuropathology shows clear regional differences in many brain diseases. For example, brains from cerebral malaria (CM) patients show more hemorrhagic punctae in the brain’s white matter (WM) than grey matter (GM). The underlying reason for these differential pathologies is unknown. Here, we assessed the effect of the vascular microenvironment on brain endothelial phenotype, focusing endothelial protein C receptor (EPCR). We demonstrate that the basal level of EPCR expression in cerebral microvessels is heterogeneous in the WM compared to the GM. We used in vitro brain endothelial ce

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Staunton, Michael, Cathy Drexler, Michael G. Dulitz, Dale C. Ekbom, William T. Schmeling, and Neil E. Farber. "Effects of Hypoxia–Reoxygenation on Microvascular Endothelial Function in the Rat Hippocampal Slice." Anesthesiology 91, no. 5 (1999): 1462. http://dx.doi.org/10.1097/00000542-199911000-00040.

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Background Cerebral ischemia and hypoxia may cause injury to both neuronal and vascular tissue. The direct effects of hypoxia on endothelial function in intraparenchymal cerebral arterioles are unknown. Using a modification of the rat brain slice preparation, allowing continuous imaging of these previously inaccessible vessels, microvessel dilation was evaluated before and after a brief hypoxic episode. Methods Rat brain slices were superfused with oxygenated artificial cerebrospinal fluid. Hippocampal arterioles were visualized using computerized videomicroscopy, and their diameters (range, 1

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Beard, Richard S., Jason J. Reynolds, and Shawn E. Bearden. "Hyperhomocysteinemia increases permeability of the blood-brain barrier by NMDA receptor-dependent regulation of adherens and tight junctions." Blood 118, no. 7 (2011): 2007–14. http://dx.doi.org/10.1182/blood-2011-02-338269.

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Abstract Hyperhomocysteinemia (HHcy) increases permeability of the blood-brain barrier, but the mechanisms are undetermined. Homocysteine (Hcy) is an agonist of the neuronal N-methyl-D-aspartate receptor (NMDAr). We tested the hypothesis that HHcy disrupts the blood-brain barrier by an NMDAr-dependent mechanism in endothelium. In brain microvascular endothelial cells, there was no change in expression of the adherens junction protein VE-cadherin with Hcy treatment, but there was a significant decrease in the amount of β-catenin at the membrane. Moreover, Hcy caused nuclear translocation of β-c

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Chandra, Partha K., Ibolya Rutkai, Hogyoung Kim, et al. "Latent HIV-Exosomes Induce Mitochondrial Hyperfusion Due to Loss of Phosphorylated Dynamin-Related Protein 1 in Brain Endothelium." Molecular Neurobiology 58, no. 6 (2021): 2974–89. http://dx.doi.org/10.1007/s12035-021-02319-8.

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AbstractDamage to the cerebral vascular endothelium is a critical initiating event in the development of HIV-1-associated neurocognitive disorders. To study the role of mitochondria in cerebral endothelial dysfunction, we investigated how exosomes, isolated from both cell lines with integrated provirus and HIV-1 infected primary cells (HIV-exosomes), accelerate the dysfunction of primary human brain microvascular endothelial cells (HBMVECs) by inducing mitochondrial hyperfusion, and reducing the expression of phosphorylated endothelial nitric oxide synthase (p-eNOS). The quantitative analysis

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Lu, Tyler M., Sean Houghton, Tarig Magdeldin, et al. "Pluripotent stem cell-derived epithelium misidentified as brain microvascular endothelium requires ETS factors to acquire vascular fate." Proceedings of the National Academy of Sciences 118, no. 8 (2021): e2016950118. http://dx.doi.org/10.1073/pnas.2016950118.

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Cells derived from pluripotent sources in vitro must resemble those found in vivo as closely as possible at both transcriptional and functional levels in order to be a useful tool for studying diseases and developing therapeutics. Recently, differentiation of human pluripotent stem cells (hPSCs) into brain microvascular endothelial cells (ECs) with blood–brain barrier (BBB)-like properties has been reported. These cells have since been used as a robust in vitro BBB model for drug delivery and mechanistic understanding of neurological diseases. However, the precise cellular identity of these in

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Rom, Slava, Holly Dykstra, Viviana Zuluaga-Ramirez, Nancy L. Reichenbach, and Yuri Persidsky. "miR-98 and let-7g* Protect the Blood-Brain Barrier Under Neuroinflammatory Conditions." Journal of Cerebral Blood Flow & Metabolism 35, no. 12 (2015): 1957–65. http://dx.doi.org/10.1038/jcbfm.2015.154.

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Pathologic conditions in the central nervous system, regardless of the underlying injury mechanism, show a certain level of blood-brain barrier (BBB) impairment. Endothelial dysfunction is the earliest event in the initiation of vascular damage caused by inflammation due to stroke, atherosclerosis, trauma, or brain infections. Recently, microRNAs (miRNAs) have emerged as a class of gene expression regulators. The relationship between neuroinflammation and miRNA expression in brain endothelium remains unexplored. Previously, we showed the BBB-protective and anti-inflammatory effects of glycogen

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Vazquez-Liebanas, Elisa, Khayrun Nahar, Giacomo Bertuzzi, Annika Keller, Christer Betsholtz, and Maarja Andaloussi Mäe. "Adult-induced genetic ablation distinguishes PDGFB roles in blood-brain barrier maintenance and development." Journal of Cerebral Blood Flow & Metabolism 42, no. 2 (2021): 264–79. http://dx.doi.org/10.1177/0271678x211056395.

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Platelet-derived growth factor B (PDGFB) released from endothelial cells is indispensable for pericyte recruitment during angiogenesis in embryonic and postnatal organ growth. Constitutive genetic loss-of-function of PDGFB leads to pericyte hypoplasia and the formation of a sparse, dilated and venous-shifted brain microvasculature with dysfunctional blood-brain barrier (BBB) in mice, as well as the formation of microvascular calcification in both mice and humans. Endothelial PDGFB is also expressed in the adult quiescent microvasculature, but here its importance is unknown. We show that deleti

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Neglia, Laura, Stefano Fumagalli, Franca Orsini, Adriana Zanetti, Carlo Perego, and Maria-Grazia De Simoni. "Mannose-binding lectin has a direct deleterious effect on ischemic brain microvascular endothelial cells." Journal of Cerebral Blood Flow & Metabolism 40, no. 8 (2019): 1608–20. http://dx.doi.org/10.1177/0271678x19874509.

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Mannose-binding lectin (MBL), an initiator of the lectin pathway, is detrimental in ischemic stroke. MBL deposition on the ischemic endothelium indicates the beginning of its actions, but downstream mechanisms are not clear yet. We investigated MBL interactions with the ischemic endothelium by exposing human brain microvascular endothelial cells (hBMECs) to protocols of ischemia. Cells were exposed to hypoxia or oxygen–glucose deprivation (OGD), and re-oxygenated with human serum (HS) or recombinant MBL (rhMBL). Hypoxic hBMECs re-oxygenated with HS showed increased complement system activation

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Bhattarai, Susmita, Sudha Sharma, Utsab Subedi, et al. "The ATX–LPA Axis Regulates Vascular Permeability during Cerebral Ischemic-Reperfusion." International Journal of Molecular Sciences 23, no. 8 (2022): 4138. http://dx.doi.org/10.3390/ijms23084138.

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Endothelial permeability is a major complication that must be addressed during stroke treatment. Study of the mechanisms underlying blood–brain barrier (BBB) disruption and management of the hypoxic stress-induced permeability of the endothelium following reperfusion are both urgently needed for stroke management. Lysophosphatidic acid (LPA), a bioactive lipid essential for basic cellular functions, causes unfavorable outcomes during stroke progression. LPA-producing enzyme autotaxin (ATX) is regulated in ischemic stroke. We used an electrical cell-substrate impedance sensor (ECIS) to measure

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Watson, Ashley N., Andree-Anne Berthiaume, Anna V. Faino та ін. "Mild pericyte deficiency is associated with aberrant brain microvascular flow in aged PDGFRβ+/− mice". Journal of Cerebral Blood Flow & Metabolism 40, № 12 (2020): 2387–400. http://dx.doi.org/10.1177/0271678x19900543.

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The receptor tyrosine kinase PDGFRβ is essential for pericyte migration to the endothelium. In mice lacking one allele of PDGFRβ (PDGFRβ+/−), previous reports have described an age-dependent loss of pericytes in the brain, leading to cerebrovascular dysfunction and subsequent neurodegeneration reminiscent of that seen in Alzheimer’s disease and vascular dementia. We examined 12–20-month-old PDGFRβ+/− mice to better understand how pericyte loss affects brain microvascular structure and perfusion in vivo. We observed a mild reduction of cortical pericyte number in PDGFRβ+/− mice (27% fewer cell

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Chen, Yizhao, Osamu Tachibana, Mitsuhiro Hasegawa, et al. "Absence of Tight Junctions between Microvascular Endothelial Cells in Human Cerebellar Hemangioblastomas." Neurosurgery 59, no. 3 (2006): 660–70. http://dx.doi.org/10.1227/01.neu.0000223372.18607.d7.

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Abstract OBJECTIVE: Endothelial tight junctions form the main barrier of the blood-brain barrier (BBB). In human hemangioblastomas, cyst formation is a common and important clinical manifestation. Although most researchers consider that the cyst formation in hemangioblastomas may be caused by the breakdown of the BBB, the underlying molecular mechanisms for cyst formation remain unknown. At present, there are few reports about the change of tight junctions in microvessel endothelium of human hemangioblastomas. The purpose of this research is to investigate the change of tight junction and its

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Verbeek, M. M., J. R. Westphal, D. J. Ruiter, and R. M. de Waal. "T lymphocyte adhesion to human brain pericytes is mediated via very late antigen-4/vascular cell adhesion molecule-1 interactions." Journal of Immunology 154, no. 11 (1995): 5876–84. http://dx.doi.org/10.4049/jimmunol.154.11.5876.

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Abstract T cell adhesion to the brain microvascular endothelium and subsequent migration into the brain parenchyma is one of the major events in the development of multiple sclerosis (MS). Interactions of the T cell integrin very late antigen-4 (VLA-4) with its receptor, vascular cell adhesion molecule-1 (VCAM-1) have been described to be of crucial importance for the development of MS. We investigated the expression of these adhesion molecules in MS brain tissue by immunohistochemical analysis, and studied their functional involvement in an in vitro T cell adhesion assay. A number of other ad

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Bacic, F., S. Uematsu, R. M. McCarron, and M. Spatz. "Secretion of Immunoreactive endothelin-1 by capillary and microvascular endothelium of human brain." Neurochemical Research 17, no. 7 (1992): 699–702. http://dx.doi.org/10.1007/bf00968008.

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Greune, Lilo, Björn Kemper, Ulrich Dobrindt, et al. "Vacuolisation of human microvascular endothelial cells by enterohaemorrhagic Escherichia coli." Thrombosis and Haemostasis 102, no. 12 (2009): 1080–92. http://dx.doi.org/10.1160/th09-07-0499.

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SummaryEnterohaemorrhagic Escherichia coli (EHEC) cause haemolytic uraemic syndrome (HUS),a thrombotic microangiopathy resulting from endothelial injury in the renal glomeruli and other organs. EHEC virulence factors that damage the microvascular endothelium play therefore major roles in the pathogenesis of HUS.We identified an EHEC strain that vacuolates and kills primary human glomerular microvascular endothelial cells (GMVECs) and a human brain microvascular endothelial cell (HBMEC) line. Because the vacuolating effect closely resembles those elicited on other cells by the vacuolating cytot

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Li, Yi, Xiao-Tian Liu, Pei-Lin Zhang та ін. "Hydroxysafflor Yellow A Blocks HIF-1α Induction of NOX2 and Protects ZO-1 Protein in Cerebral Microvascular Endothelium". Antioxidants 11, № 4 (2022): 728. http://dx.doi.org/10.3390/antiox11040728.

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Zonula occludens-1 (ZO-1) is a tight junction protein in the cerebrovascular endothelium, responsible for blood–brain barrier function. Hydroxysafflor yellow A (HSYA) is a major ingredient of safflower (Carthamus tinctorius L.) with antioxidative activity. This study investigated whether HSYA protected ZO-1 by targeting ROS-generating NADPH oxidases (NOXs). HSYA administration reduced cerebral vascular leakage with ZO-1 protection in mice after photothrombotic stroke, largely due to suppression of ROS-associated inflammation. In LPS-stimulated brain microvascular endothelial cells, HSYA increa

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Coelho, Sharton V. A., Naiara M. Rust, Lucas Vellasco, et al. "Contact System Activation in Plasma from Dengue Patients Might Harness Endothelial Virus Replication through the Signaling of Bradykinin Receptors." Pharmaceuticals 14, no. 1 (2021): 56. http://dx.doi.org/10.3390/ph14010056.

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Since exacerbated inflammation and microvascular leakage are hallmarks of dengue virus (DENV) infection, here we interrogated whether systemic activation of the contact/kallikrein-kinin system (KKS) might hamper endothelial function. In vitro assays showed that dextran sulfate, a potent contact activator, failed to generate appreciable levels of activated plasma kallikrein (PKa) in the large majority of samples from a dengue cohort (n = 70), irrespective of severity of clinical symptoms. Impaired formation of PKa in dengue-plasmas correlated with the presence of cleaved Factor XII and high mol

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Barabutis, Nektarios, Mohammad S. Akhter, Mohammad A. Uddin, Khadeja-Tul Kubra, and Andrew V. Schally. "GHRH Antagonists Protect Against Hydrogen Peroxide-Induced Breakdown of Brain Microvascular Endothelium Integrity." Hormone and Metabolic Research 52, no. 05 (2020): 336–39. http://dx.doi.org/10.1055/a-1149-9347.

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AbstractGrowth hormone releasing hormone is a hypothalamic neuropeptide, which regulates the release of growth hormone from the anterior pituitary gland. Growth hormone releasing hormone antagonists are anticancer agents, associated with strong anti-inflammatory activities. In the present study, we investigated the effects of the GHRH antagonist MIA-602 in the integrity of the brain microvascular endothelium in vitro. Our observations suggest that MIA-602 protects against the H2O2-induced breakdown of the brain endothelium and enhances its integrity by inducing P53, deactivating cofilin, and s

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Li, Wei, Carmina Busu, Magdalena L. Circu, and Tak Yee Aw. "Glutathione in Cerebral Microvascular Endothelial Biology and Pathobiology: Implications for Brain Homeostasis." International Journal of Cell Biology 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/434971.

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The integrity of the vascular endothelium of the blood-brain barrier (BBB) is central to cerebrovascular homeostasis. Given the function of the BBB as a physical and metabolic barrier that buffers the systemic environment, oxidative damage to the endothelial monolayer will have significant deleterious impact on the metabolic, immunological, and neurological functions of the brain. Glutathione (GSH) is a ubiquitous major thiol within mammalian cells that plays important roles in antioxidant defense, oxidation-reduction reactions in metabolic pathways, and redox signaling. The existence of disti

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Uddin, Mohammad A., Mohammad S. Akhter, Khadeja-Tul Kubra, et al. "Hsp90 inhibition protects the brain microvascular endothelium against oxidative stress." Brain Disorders 1 (March 2021): 100001. http://dx.doi.org/10.1016/j.dscb.2020.100001.

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Pranda, Marina A., Kelsey M. Gray, Ariana Joy L. DeCastro, Gregory M. Dawson, Jae W. Jung, and Kimberly M. Stroka. "Tumor Cell Mechanosensing During Incorporation into the Brain Microvascular Endothelium." Cellular and Molecular Bioengineering 12, no. 5 (2019): 455–80. http://dx.doi.org/10.1007/s12195-019-00591-2.

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Tripathi, Abhai K., David J. Sullivan та Monique F. Stins. "Plasmodium falciparum-Infected Erythrocytes Increase Intercellular Adhesion Molecule 1 Expression on Brain Endothelium through NF-κB". Infection and Immunity 74, № 6 (2006): 3262–70. http://dx.doi.org/10.1128/iai.01625-05.

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ABSTRACT Sequestration of Plasmodium falciparum-infected erythrocytes (Pf-IRBC) in postcapillary brain endothelium is a hallmark of cerebral malaria (CM) pathogenesis. There is a correlation between adherent Pf-IRBC and increased expression of intercellular cell adhesion molecule 1 (ICAM-1), which is also a receptor for Pf-IRBC on human brain microvascular endothelial cells (HBMEC). The underlying mechanism for the increased ICAM-1 expression has not been clearly defined. Therefore, we investigated the mechanisms of ICAM-1 expression on isolated HBMEC after exposure to Pf-IRBC. Ultrastructural

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DeCastro, Ariana Joy L., Lauren Griffith, and Kimberly Stroka. "Abstract B010: The effects of tumor cell-secreted factors on endothelial cell junction phenotype." Cancer Research 83, no. 2_Supplement_2 (2023): B010. http://dx.doi.org/10.1158/1538-7445.metastasis22-b010.

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Abstract Triple negative breast cancer (TNBC) is subtype of breast cancer that has no expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). TNBC metastasizes to specific tissues such as brain and bone in a process termed organotropism. In this process, TNBC cells cross the vascular endothelium; transport across endothelial cells is, in part, regulated by cell-cell junctions. The TNBC cell secretome has been shown to contain factors such as vascular growth factor (VEGF) and matrix metalloproteinases (MMPs) that could play a role i

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Rom, Slava, Viviana Zuluaga-Ramirez, Holly Dykstra, Nancy L. Reichenbach, Servio H. Ramirez, and Yuri Persidsky. "Poly(ADP-ribose) Polymerase-1 Inhibition in Brain Endothelium Protects the Blood—Brain Barrier under Physiologic and Neuroinflammatory Conditions." Journal of Cerebral Blood Flow & Metabolism 35, no. 1 (2014): 28–36. http://dx.doi.org/10.1038/jcbfm.2014.167.

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Blood—brain barrier (BBB) dysfunction seen in neuroinflammation contributes to mortality and morbidity in multiple sclerosis, encephalitis, traumatic brain injury, and stroke. Identification of molecular targets maintaining barrier function is of clinical relevance. We used a novel in vivo model of localized aseptic meningitis where tumor necrosis factor alpha (TNFα) was introduced intracerebrally and surveyed cerebral vascular changes and leukocyte—endothelium interactions by intravital videomicroscopy. Poly(ADP-ribose) polymerase-1 (PARP) inhibition significantly reduced leukocyte adhesion t

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Bernstein, David L., Viviana Zuluaga-Ramirez, Sachin Gajghate, et al. "miR-98 reduces endothelial dysfunction by protecting blood–brain barrier (BBB) and improves neurological outcomes in mouse ischemia/reperfusion stroke model." Journal of Cerebral Blood Flow & Metabolism 40, no. 10 (2019): 1953–65. http://dx.doi.org/10.1177/0271678x19882264.

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Most neurological diseases, including stroke, lead to some degree of blood–brain barrier (BBB) dysfunction. A significant portion of BBB injury is caused by inflammation, due to pro-inflammatory factors produced in the brain, and by leukocyte engagement of the brain endothelium. Recently, microRNAs (miRNAs) have appeared as major regulators of inflammation-induced changes to gene expression in the microvascular endothelial cells (BMVEC) that comprise the BBB. However, miRNAs’ role during cerebral ischemia/reperfusion is still underexplored. Endothelial levels of miR-98 were significantly alter

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Mone, Pasquale, Jessica Gambardella, Xujun Wang, Stanislovas S. Jankauskas, Alessandro Matarese, and Gaetano Santulli. "miR-24 Targets the Transmembrane Glycoprotein Neuropilin-1 in Human Brain Microvascular Endothelial Cells." Non-Coding RNA 7, no. 1 (2021): 9. http://dx.doi.org/10.3390/ncrna7010009.

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Neuropilin-1 is a transmembrane glycoprotein that has been implicated in several processes including angiogenesis and immunity. Recent evidence has also shown that it is implied in the cellular internalization of the severe acute respiratory syndrome coronavirus (SARS-CoV-2), which causes the coronavirus disease 2019 (COVID-19). We hypothesized that specific microRNAs can target Neuropilin-1. By combining bioinformatic and functional approaches, we identified miR-24 as a regulator of Neuropilin-1 transcription. Since Neuropilin-1 has been shown to play a key role in the endothelium-mediated re

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Rigor, Robert R., Richard S. Beard, Olesya P. Litovka та Sarah Y. Yuan. "Interleukin-1β-induced barrier dysfunction is signaled through PKC-θ in human brain microvascular endothelium". American Journal of Physiology-Cell Physiology 302, № 10 (2012): C1513—C1522. http://dx.doi.org/10.1152/ajpcell.00371.2011.

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Blood-brain barrier dysfunction is a serious consequence of inflammatory brain diseases, cerebral infections, and trauma. The proinflammatory cytokine interleukin (IL)-1β is central to neuroinflammation and contributes to brain microvascular leakage and edema formation. Although it is well known that IL-1β exposure directly induces hyperpermeability in brain microvascular endothelium, the molecular mechanisms mediating this response are not completely understood. In the present study, we found that exposure of the human brain microvascular endothelium to IL-1β triggered activation of novel PKC

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d’Uscio, Livius V., Tongrong He, Anantha V. Santhanam, and Zvonimir S. Katusic. "Endothelium-specific amyloid precursor protein deficiency causes endothelial dysfunction in cerebral arteries." Journal of Cerebral Blood Flow & Metabolism 38, no. 10 (2017): 1715–26. http://dx.doi.org/10.1177/0271678x17735418.

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The exact physiological function of amyloid-β precursor protein (APP) in endothelial cells is unknown. Endothelium-specific APP-deficient (eAPP−/−) mice were created to gain new insights into the role of APP in the control of vascular endothelial function. Endothelium-dependent relaxations to acetylcholine were significantly impaired in basilar arteries of global APP knockout (APP−/−) and eAPP−/− mice ( P < 0.05). In contrast, endothelium-independent relaxations to nitric oxide (NO)-donor diethylamine-NONOate were unchanged. Western blot analysis revealed that protein expression of endothel

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Hawkins, Brian T., Richard D. Egleton, and Thomas P. Davis. "Modulation of cerebral microvascular permeability by endothelial nicotinic acetylcholine receptors." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (2005): H212—H219. http://dx.doi.org/10.1152/ajpheart.01210.2004.

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Nicotine increases the permeability of the blood-brain barrier in vivo. This implies a possible role for nicotinic acetylcholine receptors in the regulation of cerebral microvascular permeability. Expression of nicotinic acetylcholine receptor subunits in cerebral microvessels was investigated with immunofluorescence microscopy. Positive immunoreactivity was found for receptor subunits α3, α5, α7, and β2, but not subunits α4, β3, or β4. Blood-brain barrier permeability was assessed via in situ brain perfusion with [14C]sucrose. Nicotine increased the rate of sucrose entry into the brain from 0

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Othman, Basim, Leo Zeef, Tadge Szestak, et al. "Different PfEMP1-expressing Plasmodium falciparum variants induce divergent endothelial transcriptional responses during co-culture." PLOS ONE 18, no. 11 (2023): e0295053. http://dx.doi.org/10.1371/journal.pone.0295053.

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The human malaria parasite Plasmodium falciparum is responsible for the majority of mortality and morbidity caused by malaria infection and differs from other human malaria species in the degree of accumulation of parasite-infected red blood cells in the microvasculature, known as cytoadherence or sequestration. In P. falciparum, cytoadherence is mediated by a protein called PfEMP1 which, due to its exposure to the host immune system, undergoes antigenic variation resulting in the expression of different PfEMP1 variants on the infected erythrocyte membrane. These PfEMP1s contain various combin

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Wang, Zhong, Zhouqing Chen, Junjie Yang, et al. "Identification of two phosphorylation sites essential for annexin A1 in blood–brain barrier protection after experimental intracerebral hemorrhage in rats." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (2016): 2509–25. http://dx.doi.org/10.1177/0271678x16669513.

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Annexin A1 has been reported to exert a blood–brain barrier protection. This study was designed to examine the role of annexin A1 in intracerebral hemorrhage-induced blood–brain barrier dysfunction. A collagenase intracerebral hemorrhage model was performed in adult male Sprague Dawley rats. First, a possible relationship between annexin A1 and intracerebral hemorrhage pathology was confirmed by a loss of annexin A1 in the cerebrovascular endothelium and serum of intracerebral hemorrhage rats, and the rescue effects of i.v. administration of human recombinant annexin A1 in vivo and annexin A1

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Kakava, Sofia, Eveline Schlumpf, Grigorios Panteloglou, Flavia Tellenbach, Arnold von Eckardstein, and Jerome Robert. "Brain Endothelial Cells in Contrary to the Aortic Do Not Transport but Degrade Low-Density Lipoproteins via Both LDLR and ALK1." Cells 11, no. 19 (2022): 3044. http://dx.doi.org/10.3390/cells11193044.

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The transport of low-density lipoprotein (LDL) through the endothelium is a key step in the development of atherosclerosis, but it is notorious that phenotypic differences exist between endothelial cells originating from different vascular beds. Endothelial cells forming the blood–brain barrier restrict paracellular and transcellular passage of plasma proteins. Here, we systematically compared brain versus aortic endothelial cells towards their interaction with LDL and the role of proteins known to regulate the uptake of LDL by endothelial cells. Both brain endothelial cells and aortic endothe

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Alcendor, Donald. "Human Vascular Pericytes and Cytomegalovirus Pathobiology." International Journal of Molecular Sciences 20, no. 6 (2019): 1456. http://dx.doi.org/10.3390/ijms20061456.

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Pericytes are multipotent cells of the vascular system with cytoplasmic extensions proximal to endothelial cells that occur along the abluminal surface of the endothelium. The interactions between endothelial cells and pericytes are essential for proper microvascular formation, development, stabilization, and maintenance. Pericytes are essential for the regulation of paracellular flow between cells, transendothelial fluid transport, angiogenesis, and vascular immunosurveillance. They also influence the chemical composition of the surrounding microenvironment to protect endothelial cells from p

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