Relevant bibliographies by topics / Blood endothelial cells

Academic literature on the topic 'Blood endothelial cells'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Blood endothelial cells"

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Göthert, Joachim R., Sonja E. Gustin, J. Anke M. van Eekelen, Uli Schmidt, Mark A. Hall, Stephen M. Jane, Anthony R. Green, Berthold Göttgens, David J. Izon, and C. Glenn Begley. "Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium." Blood 104, no. 6 (September 15, 2004): 1769–77. http://dx.doi.org/10.1182/blood-2003-11-3952.

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Abstract Tumor growth is dependent in part on “neoangiogenesis.” Functional involvement of bone marrow (BM)-derived cells in this process has been demonstrated. However, it remains controversial as to whether tumor endothelium itself is BM derived. Here we sought to address this issue with an endothelial-specific, inducible transgenic model. We generated Cretransgenic mice (endothelial-SCL-Cre-ERT) using the tamoxifen-inducible Cre-ERT recombinase driven by the 5′ endothelial enhancer of the stem cell leukemia (SCL) locus. These mice were intercrossed with Cre reporter strains in which β-galactosidase (LacZ) or enhanced yellow fluorescent protein (EYFP) are expressed upon Cre-mediated recombination. After tamoxifen administration, endothelial LacZ staining was observed in embryonic and adult tissues. Cre-mediated recombination was also observed in newly generated tumor endothelium. In adult BM cells we could only detect trace amounts of recombination by flow cytometry. Subsequently, BM from endothelial-SCL-Cre-ERT;R26R mice was transplanted into irradiated recipients. When tumors were grown in recipient mice, which received tamoxifen, no tumor LacZ staining was detected. However, when tumors were grown in endothelial-SCL-Cre-ERT;R26R mice 3 weeks after the cessation of tamoxifen treatment, there was widespread endothelial LacZ staining present. Thus, this genetic model strongly suggests that BM cells do not contribute to tumor endothelium and demonstrates the lineage relation between pre-existing endothelium and newly generated tumor endothelial cells. (Blood. 2004;104:1769-1777)
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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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Kirsch, Torsten, Alexander Woywodt, Michaela Beese, Kristin Wyss, Joon-Keun Park, Uta Erdbruegger, Barbara Hertel, Hermann Haller, and Marion Haubitz. "Engulfment of apoptotic cells by microvascular endothelial cells induces proinflammatory responses." Blood 109, no. 7 (November 21, 2006): 2854–62. http://dx.doi.org/10.1182/blood-2006-06-026187.

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AbstractCirculating endothelial cells (CECs) have been detected in a variety of vascular disorders, but their interactions with healthy endothelium remain unknown. The aim of this study was to evaluate the response of human endothelial cells (ECs) to apoptotic or necrotic ECs in an in vitro model and to delineate pathogenetic pathways. Here we show that incubation of the human microvascular endothelial cell line (HMEC-1) with apoptotic ECs resulted in increased expression of chemokines and enhanced binding of leukocytes to HMEC-1 cells, whereas exposure of HMEC-1 cells to necrotic ECs caused no changes in leukocyte-binding affinity. Both apoptotic and necrotic cells were bound and engulfed by HMEC-1 cells and primary human umbilical vein endothelial cells (HUVECs). We therefore suggest that exposures to apoptotic and necrotic ECs induce different patterns of chemokine synthesis and leukocyte adhesion in healthy ECs. These data indicate that CECs are not only markers of vascular damage but may induce proinflammatory signals in the endothelium.
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Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (August 1994): 259–65. http://dx.doi.org/10.1046/j.1468-2982.1994.1404259.x.

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Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is synthesized within the endothelium of cerebral vessels, whereas both endothelin-1 and endothelin-3 in addition have been identified in neurons and glia. Recent electrophysiological work has suggested a neuromodulatory role for these peptides, but at present the general interest is mainly focused on their vasoactive role. Physiological stimuli such as hypoxia, anoxia, and hemodynamic shear stress will stimulate the endothelial endothelin production. In the brain, at least two types of specific subreceptors have been cloned; ETA receptors, exclusively associated with blood vessels and ETB receptors also found on glial, epithelial, and ependymal cells. The endothelins seem so far to be the most potent vasoconstrictors yet identified. The circulating plasma levels of immunoreactive endothelin are low. Since more than 80% of the total amount released from endothelial cells seems to be secreted towards the underlying smooth muscle, endothelins have been ascribed a local vasoregulatory role. Endothelins are believed to be involved in several of our most common cerebrovascular diseases and the present review comments on their possible pathophysiological role in subarachnoid haemorrhage, cerebral ischemia, and migraine.
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Speck, Nancy, Qin Zhu, Peng Gao, Joanna Tober, Laura Bennett, Changya Chen, Yasin Uzun, Yan Li, and Kai Tan. "Developmental Biology of the Blood System." Blood 134, Supplement_1 (November 13, 2019): SCI—29—SCI—29. http://dx.doi.org/10.1182/blood-2019-121283.

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Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow are derived from a small population of hemogenic endothelial (HE) cells located in the yolk sac and major caudal arteries of the mammalian embryo. HE cells undergo an endothelial to hematopoietic cell transition, giving rise to HSPCs that accumulate in intra-arterial clusters before colonizing the fetal liver. To examine the molecular transitions between endothelial cells, HE, and intra-arterial cluster cells, and the heterogeneity of HSPCs within the intra-arterial clusters, we profiled ~40,000 cells from the caudal arteries (dorsal aorta, umbilical, vitelline) of embryonic day 9.5 to 11.5 mouse embryos by single-cell RNA sequencing (scRNA-seq) and single-cell chromatin accessibility sequencing (scATAC-Seq). A continuous developmental trajectory leads from endothelial cells to intra-arterial cluster cells, with identifiable intermediate stages between endothelial cells and HE. The intermediate endothelial stages most proximal to HE are characterized by elevated expression of genes regulated by GATA and SOX transcription factors. Developmental bottlenecks separate endothelial cells from HE cells, with the efficiency of transit through one of the last bottleneck regulated by RUNX1 dosage. Distinct developmental trajectories within intra-arterial cluster cells result in two populations of CD45+HSPCs; an initial wave of multi-lineage committed progenitors followed by precursors of hematopoietic stem cells (pre-HSCs). These and other insights gained from single cell analyses of HSPC formation from arterial endothelium will be presented. Disclosures No relevant conflicts of interest to declare.
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Westerweel, Peter E., and Marianne C. Verhaar. "Protective Actions of PPAR-γActivation in Renal Endothelium." PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/635680.

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Renal endothelial damage is pivotal in the initiation and progression of renal disease. Damaged renal endothelium may be regenerated through proliferation of local endothelium and circulation-derived endothelial progenitor cells. Activation of the PPAR-γ-receptors present on endothelial cells affects their cellular behavior. Proliferation, apoptosis, migration, and angiogenesis by endothelial cells are modulated, but may involve both stimulation and inhibition depending on the specific circumstances. PPAR-γ-receptor activation stimulates the production of nitric oxide, C-type natriuretic peptide, and superoxide dismutase, while endothelin-1 production is inhibited. Together, they augment endothelial function, resulting in blood pressure lowering and direct renoprotective effects. The presentation of adhesion molecules and release of cytokines recruiting inflammatory cells are inhibited by PPAR-γ-agonism. Finally, PPAR-γ-receptors are also found on endothelial progenitor cells and PPAR-γ-agonists stimulate progenitor-mediated endothelial repair. Together, the stimulatory effects of PPAR-γ-agonism on endothelium make an important contribution to the beneficial actions of PPAR-γ-agonists on renal disease.
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Tissot Van Patot, M. C., S. MacKenzie, A. Tucker, and N. F. Voelkel. "Endotoxin-induced adhesion of red blood cells to pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L28—L36. http://dx.doi.org/10.1152/ajplung.1996.270.1.l28.

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Cell-cell interactions are important in intravascular inflammation. Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and reactive oxygen species. Red blood cells (RBC) from patients with malaria, sickle cell anemia, and diabetes also adhere to endothelial cells. The objectives of this investigation were to develop a bovine system of RBC adhesion to endothelial cells and to begin to investigate the mechanisms involved in the RBC adhesion. We show that 51Cr-RBC adhere to bovine pulmonary artery endothelial cells (BPAEC) after stimulation of both cell types with endotoxin (ETX; 50 micrograms/ml). RBC adhesion to BPAEC depended on the ETX concentration and the presence of divalent cations. TNF-alpha, IL-1 beta, and antioxidants (superoxide dismutase; catalase; and dimethyl sulfoxide) all induced RBC adhesion to BPAEC. Phosphatidylserine, which has been implicated in adhesion of sickle cells and aged RBC to endothelium, reduced RBC adhesion to BPAEC, whether ETX-treated or not. In conclusion, ETX, proinflammatory cytokines and, surprisingly, antioxidants increase RBC adherence to BPAEC monolayers. RBC adhesion to endothelium is decreased by phosphatidylserine.
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Iruela-Arispe, M. Luisa. "Pumping blood with self-reliance and cooperation." Journal of Experimental Medicine 215, no. 10 (September 18, 2018): 2480–82. http://dx.doi.org/10.1084/jem.20181537.

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In this issue of JEM, Singhal et al. (https://doi.org/10.1084/jem.20180008) explore the cellular mechanisms involved in endothelial cell regeneration in the liver. Using a combination of myeloablative and nonmyeloablative approaches, the authors found that repair of the endothelium is mediated by endothelial cells themselves, but when injured, endothelial cells enlist myeloid counterparts that aid in vascular repair.
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Smiljic, Sonja, Sladjana Savic, Zvezdan Milanovic, and Goran Grujic. "Endocardial endothelium as a blood-heart barrier." Medical review 71, no. 1-2 (2018): 60–64. http://dx.doi.org/10.2298/mpns1802060s.

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Introduction. Endocardial endothelium is formed from a single layer of closely related cells with complex interrelationships and extensive overlap at the junctional edges. Morphological characteristics of blood-heart barrier. Endocardium is composed of three layers: endocardial endothelium, subendothelial loose connective tissue and subendocardium. The fibrous component of the subendothelium consists of small amount of collagen and elastic fibers. Several cell types are present in subendocardium: telocytes, fibroblasts and nerve endings. Intercellular bonds between the endocardial endothelial cells. Endocardial endothelial cells are attached to one another via sets of binding proteins forming solid, adherent and communicating connections. Communicating connections form transmembrane channels between the neighboring cells, while solid and adherent connections form pericellular structures like stitches. The maintenance of the presumed transendocardial electrochemical potential difference provides a high gradient for certain ions as well as a selective boundary barrier, basal lamina, preventing ionic leakage. The negatively charged glycocalyx also modulates endothelial permeability. Electrophysiological characteristics of heart-blood barrier. Electrophysiological studies have shown the existence of a large number of membrane ion channels in the endocardial endothelial cells: inward rectifying K+ channels, Ca2+ dependent K+channels, voltage-dependent Cl-channels, volume-activated Cl-channels, stretch-activated cation channels and one carrier mediated transport mechanism - Na+K+adenosine triphosphatase. Conclusion. Numerous diseases of the cardiovascular system may be a consequence, but also the cause of the endocardial endothelium dysfunction. Selective damage to the endocardial endothelium and subendocardium is found in arrhythmia, atrial fibrillation, ischemia/reperfusion injury and heart failure. Typical lesions of endocardial and microvascular endothelium have also been described in sepsis, myocardial infarction, inflammation and thrombosis. The result of endothelial dysfunction is the weakening of the endothelial barrier regulation and electrolyte imbalance of the subendocardial interstitium.
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Barcia Durán, José Gabriel. "Endothelial JAK3 Expression Enhances Pro-Hematopoietic Angiocrine Function of Sinusoidal Endothelial Cells." Blood 134, Supplement_1 (November 13, 2019): 2488. http://dx.doi.org/10.1182/blood-2019-122449.

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Unlike Jak1, Jak2, and Tyk2, Jak3 is the only member of the Jak family of secondary messengers that signals exclusively by binding the common gamma chain of interleukin receptors IL2, IL4, IL7, IL9, IL15, and IL21. Jak3-null mice display defective T and NK cell development, which results in a mild SCID phenotype. Still, functional Jak3 expression outside the hematopoietic system remains unreported. Our data show that Jak3 is expressed in endothelial cells across hematopoietic and non-hematopoietic organs, with heightened expression in the bone marrow and spleen. Increased arterial zonation in the bone marrow of Jak3-null mice further suggests that Jak3 is a marker of sinusoidal endothelium, which is confirmed by fluorescent microscopy staining and single-cell RNA-sequencing. We also show that the Jak3-null niche is deleterious for the maintenance of long-term repopulating hematopoietic stem and progenitor cells (LT-HSCs) and that Jak3-overexpressing endothelial cells have increased potential to expand LT-HSCs in vitro. In addition, we identify the soluble factors downstream of Jak3 that provide endothelial cells with this functional advantage and show their localization to the bone marrow sinusoids in vivo. Our work serves to identify a novel function for a non-promiscuous tyrosine kinase in the bone marrow vascular niche and further characterize the hematopoietic stem cell niche of sinusoidal endothelium. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Blood endothelial cells"

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Al-Malki, Aysha Ibrahim. "Detection of endothelial cells in whole blood donations." Thesis, University of Sheffield, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531130.

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Yuan, Yifan. "Enhancing Blood Outgrowth Endothelial Cells for Optimal Coating of Blood Contacting Surfaces." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36837.

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Implantable cardiovascular biomaterials have been widely applied in multiple cardiovascular disorders such as coronary artery disease, heart failure, and abdominal aortic aneurysms. However the failure modes of cardiovascular biomaterials are not uncommon, which is mainly due to the complications on blood-contacting surfaces such as thrombosis, calcification, and inflammation. Endothelium locates the inner surface of vessel lumen and is a critical regulator of vascular homeostasis. However, a readily available functional autologous source of endothelium has been hard to achieve. Human blood outgrowth endothelial cells (BOECs), cultured from peripheral blood mononuclear cells are proliferative and express endothelial protein profiles and as such are a very promising novel cell source for cardiovascular biomaterials coating. Endothelial nitric oxide synthase (eNOS) is an important regulator of vascular homeostasis and loss of eNOS activity is a hallmark of endothelial dysfunction. My data demonstrated that BOECs express markedly lower eNOS protein, mRNA as well as activity levels when compared to mature endothelial cells (ECs). My first project was to use transient transfection methods along with minicircle DNA to enhance eNOS expression levels in BOECs. Two promoters were tested in BOECs, the CMV promoter (pMini-CMV-eNOS) and the EF1α promoter (pMini-EF1α-eNOS). Transfection with pMini-CMV-eNOS achieved 24.8 ± 5.1 times more eNOS expression when compared to null transfected cells at 24 hours, a marked improvement over that achieved with conventional PVAX plasmid (10.2 ± 4.7 fold increase) or pMini-EF1α-eNOS (8.2 ± 1.2 fold increase both compared to null transfected control). pMini-CMV-eNOS mediated overexpression improved cell migration and network formation. When cultured on Osteopontin (OPN) coated surfaces, transient transfection with plasmid eNOS in BOECs can markedly enhance cell spreading and adhesion to ECM modified surfaces. These results suggest that eNOS expression in BOECs is suboptimal and BOECs may be functionally improved by techniques to enhance expression of this critical homeostatic regulator. Extracellular matrix (ECM) proteins have been shown to negatively regulate eNOS expression and NO production in mature ECs. In addition, the deposition of Col IV and Col I in BOECs is higher compared to that in mature ECs. Thus, I have proposed that the lower eNOS expression/activity in BOECs compared to mature ECs is due to higher ECM deposition. When grown on fibronectin, type I collagen, type IV collagen and laminin, significantly decreased eNOS protein in HUVECs were found compared to cells on polystyrene. Interestingly, when cultured on polystyrene, BOECs express significantly more extracellular matrix (ECM) proteins especially type I collagen compared to mature ECs. Blocking collagen synthesis significantly enhanced eNOS expression in BOECs (1.77 ± 0.41 fold increase). My results suggest that the regulation of eNOS in BOECs and mature ECs is similar and the reduced eNOS level in BOECs may be due to their increased collagen production. ECM proteins regulate intracellular signaling transduction primarily through integrin signaling associated with focal adhesion complexes. I have proposed that ECM proteins regulation on eNOS signaling in BOECs and mature ECs is through integrin and integrin-associated proteins. Matrix mediated eNOS downregulation was blocked by β1 integrin siRNA and focal adhesion kinase siRNA transfection in both BOECs and HUVECs. In addition, inhibitors of actin polymerization (e.g. ROCK inhibitors and cytochalasin D) block the effect of ECM on eNOS signaling. Taken together, my results suggest that ECM proteins regulate eNOS expression via a β1 integrin/FAK/actin polymerization dependent mechanism.
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Lester, Elizabeth Ann. "Consequences of biomaterial activation of blood cells on endothelial cell proinflammatory phenotype." Thesis, Georgia Institute of Technology, 2001. http://hdl.handle.net/1853/11869.

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Prasad, Raju. "Endothelial progenitor cells, vascular function, and exercise." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 59 p, 2009. http://proquest.umi.com/pqdweb?did=1654501181&sid=4&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Zolle, Lapuente Olga C. "Cyclic GMP and calcium homeostasis in endothelial cells." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367654.

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Doty, Sherry D. "Fluid shear stress effects on fibronectin in endothelial cells." Thesis, Georgia Institute of Technology, 1989. http://hdl.handle.net/1853/19073.

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Tretiach, Marina Louise. "Bovine Models of Human Retinal Disease: Effect of Perivascular Cells on Retinal Endothelial Cell Permeability." University of Sydney, 2005. http://hdl.handle.net/2123/1153.

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Doctor of Philosophy (Medicine)
Background: Diabetic vascular complications affect both the macro- and microvasculature. Microvascular pathology in diabetes may be mediated by biochemical factors that precipitate cellular changes at both the gene and protein levels. In the diabetic retina, vascular pathology is found mainly in microvessels, including the retinal precapillary arterioles, capillaries and venules. Macular oedema secondary to breakdown of the inner blood-retinal barrier is the most common cause of vision impairment in diabetic retinopathy. Müller cells play a critical role in the trophic support of retinal neurons and blood vessels. In chronic diabetes, Müller cells are increasingly unable to maintain their supportive functions and may themselves undergo changes that exacerbate the retinal pathology. The consequences of early diabetic changes in retinal cells are primarily considered in this thesis. Aims: This thesis aims to investigate the effect of perivascular cells (Müller cells, RPE, pericytes) on retinal endothelial cell permeability using an established in vitro model. Methods: Immunohistochemistry, cell morphology and cell growth patterns were used to characterise primary bovine retinal cells (Müller cells, RPE, pericytes and endothelial cells). An in vitro model of the blood-retinal barrier was refined by coculturing retinal endothelial cells with perivascular cells (Müller cells or pericytes) on opposite sides of a permeable Transwell filter. The integrity of the barrier formed by endothelial cells was assessed by transendothelial electrical resistance (TEER) measurements. Functional characteristics of endothelial cells were compared with ultrastructural morphology to determine if different cell types have barrier-enhancing effects on endothelial cell cultures. Once the co-culture model was established, retinal endothelial cells and Müller cells were exposed to different environmental conditions (20% oxygen, normoxia; 1% oxygen, hypoxia) to examine the effect of perivascular cells on endothelial cell permeability under reduced oxygen conditions. Barrier integrity was assessed by TEER measurements and permeability was measured by passive diffusion of radiolabelled tracers from the luminal to the abluminal side of the endothelial cell barrier. A further study investigated the mechanism of laser therapy on re-establishment of retinal endothelial cell barrier integrity. Müller cells and RPE, that comprise the scar formed after laser photocoagulation, and control cells (Müller cells and pericytes, RPE cells and ECV304, an epithelial cell line) were grown in long-term culture and treated with blue-green argon laser. Lasered cells were placed underneath confluent retinal endothelial cells growing on a permeable filter, providing conditioned medium to the basal surface of endothelial cells. The effect of conditioned medium on endothelial cell permeability was determined, as above. Results: Co-cultures of retinal endothelial cells and Müller cells on opposite sides of a permeable filter showed that Müller cells can enhance the integrity of the endothelial cell barrier, most likely through soluble factors. Low basal resistances generated by endothelial cells from different retinal isolations may be the result of erratic growth characteristics (determined by ultrastructural studies) or the selection of vessel fragments without true ‘barrier characteristics’ in the isolation step. When Müller cells were co-cultured in close apposition to endothelial cells under normoxic conditions, the barrier integrity was enhanced and permeability was reduced. Under hypoxic conditions, Müller cells had a detrimental effect on the integrity of the endothelial cell barrier and permeability was increased in closely apposed cells. Conditioned medium from long-term cultured Müller cells and RPE that typically comprise the scar formed after lasering, enhanced TEER and reduced permeability of cultured endothelial cells. Conclusions: These studies confirm that bovine tissues can be used as a suitable model to investigate the role of perivascular cells on the permeability of retinal endothelial cells. The dual effect of Müller cells on the retinal endothelial cell barrier under different environmental conditions, underscores the critical role of Müller cells in regulating the blood-retinal barrier in health and disease. These studies also raise the possibility that soluble factor(s) secreted by Müller cells and RPE subsequent to laser treatment reduce the permeability of retinal vascular endothelium. Future studies to identify these factor(s) may have implications for the clinical treatment of macular oedema secondary to diseases including diabetic retinopathy.
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Ahmed, Syed Rumel. "Characterising lymphocyte trafficking across blood vascular and lymphatic endothelial cells." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3846/.

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The recruitment of peripheral blood lymphocytes (PBL) to sites of inflammation and their subsequent traffic into the lymphatic circulation is important in host defense. However, surprisingly little is known about their recruitment from the blood vasculature into inflamed tissue, and almost nothing about their egress from inflamed tissue via the lymphatic circulation. We showed that both human macrovascular and microvascular endothelial cells stimulated by TNF\(\alpha\) and IFN\(\gamma\), preferentially recruited memory T-lymphocytes (CD45RO positive cells) from a mixed pool of PBL. T-cells that had migrated across vascular endothelial cells subsequently utilised a combination of \(\beta\)1 and \(\beta\)2 integrins to traverse cytokine activated lymphatic endothelium. In addition we provide evidence that PGD2 was critical for the transmigration of lymphocytes through vascular endothelium. The process of trans-lymphatic migration was also significantly retarded in the presence of a function neutralising antibody against CCR7. Most importantly, we observed that memory T-cells showed a markedly enhanced capacity to migrate across lymphatic endothelium if they had first traversed a vascular endothelial cell barrier. We have shown that addition of exogenous PGD2 to isolated lymphocytes is able to restore the enhanced migration capacity of lymphocytes that have previously migrated through a vascular monolayer. The nature of the priming signal delivered by the process of migration across blood vessel endothelium remains to be fully identified, but is likely to be important in regulating the dynamics of an inflammatory response.
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Helmlinger, Gabriel. "Effects of pulsatile laminar shear stress on cultured vascular endothelial cells." Thesis, Georgia Institute of Technology, 1990. http://hdl.handle.net/1853/16738.

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Seetharaman, Seeta Lakshmy. "Multidrug transporter expression in endothelial cells of the blood-brain barrier." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621690.

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Books on the topic "Blood endothelial cells"

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Ricard, Cervera, Khamashta Munther A. A, and Hughes Graham R. V, eds. Antibodies to endothelial cells and vascular damage. Boca Raton, Fla: CRC Press, 1994.

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Kelleher, Siobhan. Signal transduction by endothelial cells: Investigation of early effects. Dublin: University College Dublin, 1998.

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Herrera, Esperanza Meléndez, Bryan V. Phillips-Farfán, and Gabriel Gutiérrez Ospina. Endothelial cell plasticity in the normal and injured central nervous system. Boca Raton: CRC Press/Taylor & Francis, 2015.

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1959-, Lewis Thomas J., and Robinson James 1958-, eds. Angiogenesis research progress. New York: Nova Science Publishers, 2008.

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L, Gordon J., ed. Vascular endothelium: Interactions with circulating cells. Amsterdam: Elsevier, 1991.

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W, Siemann Dietmar, ed. Vascular-targeted therapies in oncology. Chichester, West Sussex: J. Wiley, 2006.

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E, Sumpio Bauer, ed. Hemodynamic forces and vascular cell biology. Austin, Tex: R.G. Landes, 1993.

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Modeling tumor vasculature: Molecular, cellular, and tissue level aspects and implications. New York: Springer, 2012.

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Triton Biosciences-UCLA Symposium (1985 Park City, Utah). Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of a Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. Edited by Edgington Thomas S, Ross Russell, and Silverstein Samuel C. New York, N.Y: A.R. Liss, 1987.

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S, Edgington Thomas, Ross Russell, and Silverstein Samuel C, eds. Perspectives in inflammation, neoplasia, and vascular cell biology: Proceedings of the Triton Biosciences-UCLA Symposium, held in Park City, Utah, February 2-8, 1985. New York: Liss, 1987.

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Book chapters on the topic "Blood endothelial cells"

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Edelman, Elazer. "Endothelial Cells and Hemodynamics." In McDonald's Blood Flow in Arteries, 125–35. 7th ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781351253765-5.

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Mund, Julie, David A. Ingram, and Mervin C. Yoder. "Defining Endothelial Progenitor Cells." In Regenerative Therapy Using Blood-Derived Stem Cells, 9–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-471-1_2.

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Risau, Werner. "Development of Blood-Brain Barrier Endothelial Cells." In Biology and Physiology of the Blood-Brain Barrier, 1–7. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_1.

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Ribatti, Domenico. "Tumor Blood Vessels and Tumor Endothelial Cells." In The Role of Microenvironment in the Control of Tumor Angiogenesis, 11–18. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27820-9_2.

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Zozulya, Alla, Christian Weidenfeller, and Hans-Joachim Galla. "Induction of Blood-Brain Barrier Properties in Cultured Endothelial Cells." In Blood-Brain Barriers, 357–74. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2007. http://dx.doi.org/10.1002/9783527611225.ch16.

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Hibbert, Benjamin, Trevor Simard, and Edward R. O’Brien. "Endothelial Progenitors and Repair of Cardiovascular Disease." In Regenerative Therapy Using Blood-Derived Stem Cells, 97–107. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-471-1_8.

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Kefalides, Nicholas A. "Response of Blood Vessel Cells to Viral Infection." In Endothelial Cell Biology in Health and Disease, 431–49. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0937-6_19.

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Ando, Joji, Shigenobu Araya, Youichi Katayama, Akira Ohtsuka, and Akira Kamiya. "Flow-Induced Calcium Response in Cultured Vascular Endothelial Cells." In Regulation of Coronary Blood Flow, 230–41. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68367-4_19.

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Weber, Benedikt, Steffen M. Zeisberger, and Simon P. Hoerstrup. "Umbilical Cord Blood-Derived Endothelial Progenitor Cells for Cardiovascular Tissue Engineering." In Perinatal Stem Cells, 325–36. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1118-9_29.

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Langille, B. L., A. I. Gotlieb, and D. W. Kim. "In vivo Responses of Endothelial Cells to Hemodynamic Stress." In Role of Blood Flow in Atherogenesis, 157–61. Tokyo: Springer Japan, 1988. http://dx.doi.org/10.1007/978-4-431-68399-5_23.

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Conference papers on the topic "Blood endothelial cells"

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Szatmary, Alex C., Rohan J. Banton, and Charles D. Eggleton. "Deformation of White Blood Cells Firmly Adhered to Endothelium." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80894.

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Circulating white blood cells adhere to endothelium near an infection site; this occurs because infection causes ligands to be expressed on activated endothelium. Initially, a white blood cell rolls on the substrate, but eventually forms a firm adhesion, allowing it to crawl through the endothelial layer toward the infected tissue. A computational model of bond kinetics, cell deformability, and fluid dynamics was used to model the forces experienced by a cell during this process. The cell was modeled as a fluid-filled membrane; on its surface were hundreds of deformable microvilli—little fingers, ruffles in the white blood cell’s wrinkly membrane. These microvilli were deformable and their tips were decorated with PSGL-1 chemical receptors which bound to P-selectin ligands on the surface. Softer cells and cells subjected to higher fluid shear stress deformed more, and having more contact area, they formed more bonds and were able to resist more hydrodynamic load.
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Lim, Yi Chung, and David S. Long. "Aortic Hemodynamics and Endothelial Gene Expression: An Animal Specific Approach." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53312.

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Atherosclerosis is a major cause of morbidity and mortality in the developed world. This disease is identified by endothelial dysfunction, inflammation and the accumulation of lipids and cellular elements within the intima of medium and large-sized arteries. Within these arteries, the distribution of atherosclerotic lesions is non-uniform; the inner wall of curved sections and the outer walls of bifurcations are susceptible sites. Evidence suggests that the focal nature of the disease is mediated in part by local fluid mechanical stresses at the interface between flowing blood and the vessel wall. Strategically located at this interface is the monolayer of cells known as the endothelium. Although it was once considered to be an inert cell layer, the endothelium is a highly complex and metabolically dynamic cell layer. As a result, local fluid mechanical stresses at the wall of arteries may alter the phenotype of endothelial cells (ECs). With that in mind, the aim of this study is to better characterize the modulation of the endothelial cell phenotype in response to blood flow induced wall shear stress (WSS).
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Ting, Lucas H., and Nathan J. Sniadecki. "Hemodynamic Shear Regulates Intercellular Forces and Permeability of Endothelial Cell Monolayers." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80789.

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In the cardiovascular system, the flow of blood within the complex vascular network creates hemodynamic shear forces experienced by cells. Situated between the circulating blood and the bulk vascular tissue, the endothelium is a cell monolayer acting as a barrier that protects the underlying arterial tissue. Shear forces have been seen to interact with and regulate endothelial cells through mechanotransduction induced cytoskeletal changes within the cell [1]. Shear forces can be beneficial in cases of laminar flow, which are thought to be atheroprotective by aligning and organizing endothelial cells [2]. However, disturbances to a smooth flow field, caused by vessel bifurcations or obstructions like an implanted stent or a bulging atherosclerotic lesion, can cause recirculation zones to form downstream. In these flow regions, detrimental monolayer remodeling occurs which breaks down the endothelial barrier function [3]. Biochemically, it has been seen that shear forces drive signaling cascades in the Rho/Rac pathways that cascade into morphological changes in the cytoskeleton [4].
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Segawa, Naoki, and Yasuhiko Sugii. "Velocity Measurement of In Vitro Blood Flow in Microchip Cultured Endothelial Cells." In ASME 2008 First International Conference on Micro/Nanoscale Heat Transfer. ASMEDC, 2008. http://dx.doi.org/10.1115/mnht2008-52250.

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In order to investigate vascular diseases such as cause of atherosclerosis and myocardial infarction, relationships of endothelial cells (ECs) covered with surface blood vessels and blood flow stimulation have been experimentally studied. In the study, a blood vessel model for in vitro experiment made from polydimethylsiloxane (PDMS) microchip with a straight microchannel with 400 μm width and 100 μm depth was developed. By optimizing cells cultured condition such as the liquid introduction method and the surface coating for enhancement of cell attachment on the microchannel wall, cell culture method in the microchip were developed. Velocity distributions on the ECs surface in the blood vessel model were measured using micro PIV technique. Measured velocity vectors on the ECs surface were fluctuated caused by the three dimensional effect of the cell shape.
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Ahsan, Taby, Adele M. Doyle, Garry P. Duffy, Frank Barry, and Robert M. Nerem. "Stem Cells and Vascular Regenerative Medicine." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193591.

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Vascular applications in regenerative medicine include blood vessel substitutes and vasculogenesis in ischemic or engineered tissues. For these repair processes to be successful, there is a need for a stable supply of endothelial and smooth muscle cells. For blood vessel substitutes, the immediate goal is to enable blood flow, but vasoactivity is necessary for long term success. In engineered vessels, it is thought that endothelial cells will serve as an anti-thrombogenic lumenal layer, while smooth muscle cells contribute to vessel contractility. In other clinical applications, what is needed is not a vessel substitute but the promotion of new vessel formation (vasculogenesis). A simplified account of vasculogenesis is that endothelial cells assemble to form vessel-like structures that can then be stabilized by smooth muscle cells. Overall, the need for new vasculature to transfer oxygen and nutrients is important to reperfuse not only ischemic tissue in vivo, but also dense, structurally complex engineered tissue. The impact of these vascular therapies, however, is limited in part by the low yield and inadequate in vitro proliferation potential of primary endothelial and smooth muscle cells. Thus, there is a need to address the cell sourcing issue for vascular cell-based therapies, potentially using stem cells.
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Lan, Sheeny K., Daniel N. Prater, Russell D. Jamison, David A. Ingram, Mervin C. Yoder, and Amy J. Wagoner Johnson. "Vasculogenic Potential of Porcine Endothelial Colony Forming Cells." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192848.

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The natural healing process cannot restore form and function to critical size bone defects without the presence of a graft to support and guide tissue regeneration [1]. Critical size bone defects in humans are typically on the order of centimeters or larger [2]. Thus, a major limitation of synthetic grafts or bone tissue engineering constructs is the lack of vascularization to support cell viability after placement in vivo [3]. Cells that participate in bone regeneration, must reside within 150–200 microns of a blood supply in order to gain proper nutrients and to eliminate waste [4]. Consequently, a tissue engineering construct of a clinically relevant size cannot rely on diffusion for transport of nutrients and waste. Previous research has shown that blood vessels can infiltrate scaffolds, but the overall process is too slow to prevent death of cells located in the center of a construct [5].
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Schen, Aaron, Baoguo Chen, and Lisa X. Xu. "Preliminary Study of Vascular Endothelial Ca2+ Response to Elevated Temperature." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/htd-24424.

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Abstract Local hyperthermia has been the subject of much research because of its great potential for therapeutic and clinic applications. It has been long recognized that a major factor, which affects tissue temperature elevation and heterogeneity during hyperthermia, is the augmentation of blood flow concomitant with the heating. The heat-induced change in local blood flow can be attributed to sympathetically mediated re-distribution of cardiac output and change in local flow resistance resulting from thermally stimulated regulation in diameters of arterioles. It has been found that the vascular endothelium significantly affects the dynamic response of the vessel diameter to thermal stimuli. Endothelial cells play key regulatory roles by producing several potent vasoactive agents and regulating coagulation states, i.e. endothelium derived relaxing factors (EDRFs). Most endothelial functions depend to various extents on changes in intracellular calcium concentration [Ca2+]i. A new approach to studying vascular thermo-regulation during hyperthermia has been developed in this research to quantitatively measure the dynamic response of vascular endothelial Ca2+ to temperature elevations using confocal fluorescence ratio imaging. The cell membrane permeable fluorescence dye Fura-2/AM esters were loaded into the vascular endothelial cells and ratio imaging of the fluorescent endothelial cell were taken under the excitation of 334 and 380nm wavelengths. The signal intensities were calibrated with the endothelial calcium ion concentration ([Ca2+]i) and temperatures ranged from 37°C to 44°C. This calibration will provide a means to quantitatively measure the vascular endothelial [Ca2+]i transients in in vivo tissue when subjected to temperature elevations from 38°C to 44°C, and thus to further understand the role of endothelium in thermally induced vascular regulation under hyperthermic conditions in the near future.
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Kemeny, Steven F., and Alisa Morss Clyne. "High Glucose Alters Endothelial Cell Response to Shear Stress." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206531.

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Endothelial cells line the walls of all blood vessels, where they maintain homeostasis through control of vascular tone, permeability, inflammation, and the growth and regression of blood vessels. Endothelial cells are mechanosensitive to fluid shear stress, elongating and aligning in the flow direction [1–2]. This shape change is driven by rearrangement of the actin cytoskeleton and focal adhesions [2]. Hyperglycemia, a hallmark of diabetes, affects endothelial cell function. High glucose has been shown to increase protein kinase C, formation of glucose-derived advanced glycation end-products, and glucose flux through the aldose reductase pathway within endothelial cells [3]. These changes are thought to be related to increased reactive oxygen species production [4]. While endothelial cell mechanics have been widely studied in healthy conditions, many disease states have yet to be explored. Biochemical alterations related to high glucose may alter endothelial cell mechanics.
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Fukushima, Shuichiro, Kenichiro Inagi, Kotaro Oka, and Kazuo Tanishita. "Measurement of Micro Flow Field Over Model Endothelial Cells." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0228.

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Abstract Shear stress induced by blood flow on the arterial wall affect morphology and physiology of endothelial cells. The specific mechanisms alternating shapes and functions have not been identified in endothelial cells, because of the lack of a detailed description of the flow near the cell surface. Although the velocity profiles were numerically calculated (Barbee et al., 1995, Satcher et al., 1992, Yamamoto et al., 1996), experimental verification has not been accomplished.
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Huertas, A., S. Das, J. Lindert, M. Yiming, S. Canfield, S. Bhattacharya, and J. Bhattacharya. "Red Blood Cells Induce Proinflammatory Lung Endothelial Signaling in Hypoxia." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5562.

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Reports on the topic "Blood endothelial cells"

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

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infarction, kidney failure, among others. Cardiovascular complications have been reported to derive from dysfunction of endothelial cells, which have important functions in blood vessels. In order to understand the etiology of this poor function of endothelial cells, it is necessary to study the molecular mechanisms involved in these functions, to identify the effects of diabetes and thus, develop new research that will mitigate the effects of this pathology.
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