Relevant bibliographies by topics / Endothelium

Academic literature on the topic 'Endothelium'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "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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Luscher, TF, and Y. Dohi. "Endothelium-Derived Relaxing Factor and Endothelin in Hypertension." Physiology 7, no. 3 (June 1, 1992): 120–23. http://dx.doi.org/10.1152/physiologyonline.1992.7.3.120.

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In resistance arteries, endothelium-derived nitric oxide inhibits vasoconstrictors;this and endothelium-dependent relaxations to acetylcholine are blunted in hypertension. The sensitivity of hypertensive resistance arteries with endothelium to intraluminal endothelin-1 is normal but is reduced without endothelium. Thus hypertension impairs endothelial regulation of the resistance circulation.
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Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.

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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immunoreactivity were measured by radioimmunoassay in the supernatants of corpus cavernosum endothelial cells in culture. Endothelins are potent constrictors and caused long-lasting contractions of corporeal strips in organ chambers. Equilibrium binding analysis of endothelins to their receptor sites revealed high-affinity, specific, and saturable binding of labeled endothelins to corporeal membranes. Competition binding experiments demonstrated receptors with high affinity for ET-1 and -2 and low affinity for ET-3 and another, less abundant, set of receptors with high affinity for ET-1, -2, and -3. Affinity labeling of endothelins to corporeal membranes, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, revealed that ET-1 and -2 cross-linked specifically to three different molecular mass components (75, 52, and 34 kDa). ET-3 bound only to the 34-kDa component. It is concluded that human corpus cavernosum endothelium has the ability to synthesize and release endothelin, that endothelins contract corporeal smooth muscle, and that at least two distinct endothelin receptors may exist and are differentiated by their affinity for ET-3.
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Wang, Xuemei, Yanlin Zhong, Minghui Liang, Zhirong Lin, Huping Wu, and Cheng Li. "Crosslinking-Induced Corneal Endothelium Dysfunction and Its Protection by Topical Ripasudil Treatment." Disease Markers 2022 (January 13, 2022): 1–12. http://dx.doi.org/10.1155/2022/5179247.

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Purpose. To investigate the changes of corneal endothelium under different crosslinking conditions and the protective effect of ripasudil. Methods. Corneal crosslinking groups were infiltrated with riboflavin and subsequently irradiated with 0.54 J/cm2 or 1.08 J/cm2 UVA, while noncrosslinking groups included neither UVA nor riboflavin treatment, only 1.08 J/cm2 UVA and only riboflavin treatment. Corneal opacity, variations in corneal endothelial cells, and corneal thickness of all groups were observed by slit lamp, in vivo confocal microscopy, and optical coherence tomography. Immunofluorescence staining and scanning electron microscopy were performed to evaluate changes in the structure and function of the corneal endothelium. The mice that received a corneal crosslinking dose of 1.08 J/cm2 were instilled with ripasudil to explore its protective effect on the corneal endothelium. Results. Treatment with UVA and riboflavin caused an increase in corneal opacity and corneal thickness and decreased endothelial cell density. Furthermore, treatment with UVA and riboflavin caused endothelial cell DNA damage and destroyed the tight junction and pump function of the endothelium, while riboflavin or the same dose of UVA alone did not affect the endothelium. Ripasudil reduced DNA damage in endothelial cells, increased the density of cells, and protected the endothelium’s integrity and function. Conclusion. Riboflavin combined with UVA can damage the corneal endothelium’s normal functioning. The corneal endothelium’s wound healing is dose-dependent, and the ROCK inhibitor ripasudil maintains the endothelium’s pump and barrier functions.
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Xiao, Hongbo, Jun Fang, Xiangyang Lu, Zhikui Liu, Xiaojun Chen, Jinhui Liu, Jianming Su, Jine Yi, and Zhiliang Sun. "Protective effect of soluble fiber from Undaria pinnatifida on vascular endothelium in hypercholesterolemic rabbits." Canadian Journal of Animal Science 89, no. 3 (September 1, 2009): 361–67. http://dx.doi.org/10.4141/cjas08132.

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Dietary fiber could improve endothelial function and abnormal production of nitric oxide (NO) and elevated endothelin-1 (ET-1) concentration induce endothelial dysfunction. In the present study, we tested the effect of soluble fiber extracted from Undaria pinnatifida (UP) on endothelial function and NO and ET-1 production in hypercholesterolemic rabbits. After treatment with UP soluble fiber (5 or 10%) for 8 wk, endothelium-dependent vasorelaxation in isolated aortic rings, the concentrations of NO and ET-1 and malondialdehyde (MDA), and the expression of endothelial NO synthase (eNOS) gene were measured. The UP soluble fiber (5 or 10%) treatment significantly attenuated the impairment of endothelium-dependent vasorelaxation concomitantly with increase of plasma NO concentration and expression of aortic endothelial nitric oxide synthase (eNOS), reduction of plasma MDA level and ET-1 concentration and aortic ET-1 concentration. The present study indicates that the protective effects of UP soluble fiber on endothelium-mediated vasorelaxation may be related to an improved NO production and a reduced ET-1 concentration in hypercholesterolemic rabbits.Key words: Undaria pinnatifida, soluble fiber, endothelium, nitric oxide, endothelin-1, rabbit
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Tanner, Felix C., Marcel R. Tschudi, and Thomas F. Lüscher. "Endothelium, lipoproteins and atherosclerotic vascular disease." Vascular Medicine Review vmr-2, no. 2 (September 1991): 161–76. http://dx.doi.org/10.1177/1358836x9100200207.

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The endothelium modulates vascular tone by releasing nitric oxide, which is a potent vasodilator and inhibitor of platelet aggregation. Together with prostacyclin, the endogenous nitrate nitric oxide has an important protective role in preventing vasospasm and thrombus formation. In addition, the endothelium is a source of contracting factors such as endothelin-1, thromboxane A2 and endoperoxides. Due to its strategic anatomical position, the endothelium is a primary target for injurious stimuli and cardiovascular risk factors. Low density lipoproteins reduce endothelium-dependent relaxation and enhance endothelium- dependent contraction. The same pattern of endothelial dysfunction occurs in hypercholesterolaemia and atherosclerosis. These alterations of endothelial function may contribute to vasospasm, ischaemia and thrombus formation, which are common events in patients with atherosclerotic vascular disease.
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Marsden, P. A., M. S. Goligorsky, and B. M. Brenner. "Endothelial cell biology in relation to current concepts of vessel wall structure and function." Journal of the American Society of Nephrology 1, no. 7 (January 1991): 931–48. http://dx.doi.org/10.1681/asn.v17931.

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Vascular endothelium is now appreciated to modulate vessel wall structure and function in health and disease. Strategically located between the intravascular space and vessel wall proper, the endothelium has a broad capacity to modify the functional state of adjacent or trafficking cells. Furthermore, recent findings indicate that the endothelium is an interactive tissue capable of responding to numerous mechanical, chemical, and cellular stimuli. The focus of this review will be a discussion of endothelial cell biology in relation to vascular structure and function, with particular emphasis on endothelial modulation of vasomotor tone. It is evident that endothelial cells contribute to the local control of vascular tone by releasing potent vasodilatory mediators, such as endothelium-derived relaxing factor, and vasoconstrictor mediators such as endothelin-1. The endothelium also serves to modify blood-borne signals to which vascular tissues respond. The kidney shares, directly and indirectly, in these events, making this emerging new area a focus of major interest for nephrologists.
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Yang, Qingliang, Harshani Wijerathne, Jordan C. Langston, Mohammad F. Kiani, and Laurie E. Kilpatrick. "Emerging Approaches to Understanding Microvascular Endothelial Heterogeneity: A Roadmap for Developing Anti-Inflammatory Therapeutics." International Journal of Molecular Sciences 22, no. 15 (July 21, 2021): 7770. http://dx.doi.org/10.3390/ijms22157770.

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The endothelium is the inner layer of all blood vessels and it regulates hemostasis. It also plays an active role in the regulation of the systemic inflammatory response. Systemic inflammatory disease often results in alterations in vascular endothelium barrier function, increased permeability, excessive leukocyte trafficking, and reactive oxygen species production, leading to organ damage. Therapeutics targeting endothelium inflammation are urgently needed, but strong concerns regarding the level of phenotypic heterogeneity of microvascular endothelial cells between different organs and species have been expressed. Microvascular endothelial cell heterogeneity in different organs and organ-specific variations in endothelial cell structure and function are regulated by intrinsic signals that are differentially expressed across organs and species; a result of this is that neutrophil recruitment to discrete organs may be regulated differently. In this review, we will discuss the morphological and functional variations in differently originated microvascular endothelia and discuss how these variances affect systemic function in response to inflammation. We will review emerging in vivo and in vitro models and techniques, including microphysiological devices, proteomics, and RNA sequencing used to study the cellular and molecular heterogeneity of endothelia from different organs. A better understanding of microvascular endothelial cell heterogeneity will provide a roadmap for developing novel therapeutics to target the endothelium.
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Ricard, Nicolas, Rizaldy P. Scott, Carmen J. Booth, Heino Velazquez, Nicholas A. Cilfone, Javier L. Baylon, Jeffrey R. Gulcher, Susan E. Quaggin, Thomas W. Chittenden, and Michael Simons. "Endothelial ERK1/2 signaling maintains integrity of the quiescent endothelium." Journal of Experimental Medicine 216, no. 8 (June 13, 2019): 1874–90. http://dx.doi.org/10.1084/jem.20182151.

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To define the role of ERK1/2 signaling in the quiescent endothelium, we induced endothelial Erk2 knockout in adult Erk1−/− mice. This resulted in a rapid onset of hypertension, a decrease in eNOS expression, and an increase in endothelin-1 plasma levels, with all mice dying within 5 wk. Immunostaining and endothelial fate mapping showed a robust increase in TGFβ signaling leading to widespread endothelial-to-mesenchymal transition (EndMT). Fibrosis affecting the cardiac conduction system was responsible for the universal lethality in these mice. Other findings included renal endotheliosis, loss of fenestrated endothelia in endocrine organs, and hemorrhages. An ensemble computational intelligence strategy, comprising deep learning and probabilistic programing of RNA-seq data, causally linked the loss of ERK1/2 in HUVECs in vitro to activation of TGFβ signaling, EndMT, suppression of eNOS, and induction of endothelin-1 expression. All in silico predictions were verified in vitro and in vivo. In summary, these data establish the key role played by ERK1/2 signaling in the maintenance of vascular normalcy.
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Auguet, Michel, Sylvie Delaflotte, Pierre-Etienne Chabrier, and Pierre Braquet. "Characterization of endothelin receptors mediating contraction and relaxation in rabbit saphenous artery and vein." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (October 1, 1993): 818–23. http://dx.doi.org/10.1139/y93-122.

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The endothelin receptors in rabbit isolated rings of saphenous artery and saphenous vein have been characterized using endothelin-1, endothelin-2, endothelin-3, sarafotoxin S6c, and BQ123. Although artery rings were more sensitive than those from vein to the contractile action of phenylephrine, endothelin-1 was about three times more potent as a contractile agonist on vein than on artery. In rings precontracted with phenylephrine, carbachol was 10 times more potent in vein than in artery rings to induce endothelium-dependent relaxation. However, in rings precontracted to a similar tone by endothelin-1, the relaxation elicited by carbachol was reduced in the vein but remained unchanged in the artery. In endothelium-denuded saphenous artery, endothelin-1 and endothelin-2 elicited contraction with equal potency, whereas endothelin-3 and sarafotoxin S6c were weak agonists. In saphenous vein, the rank order of sensitivity was sarafotoxin S6c > endothelin-2 > endothelin-1 = endothelin-3, whereas sarafotoxin S6c and, to a lesser extent, endothelin-3 act as partial agonists. The ETA receptor antagonist BQ123 shifted, to the right, the concentration–response curves of endothelin-1 on endothelium-denuded saphenous artery (pA2 = 7.25). In the endothelium-denuded saphenous vein, 10 μM BQ123 shifted to the right only the response to high concentrations of endothelin-1. In vein but not in artery, endothelin-1 and sarafotoxin S6c induced an endothelium-dependent relaxation, which was increased, in the case of endothelin-1, in the presence of BQ123. These results indicate that the rabbit saphenous vein contains a mixed population of ETA and ETB vasoconstrictor receptors located in the smooth muscle cells and vasorelaxant ETB receptors situated on endothelial cells. In contrast, the saphenous artery only possesses smooth muscle cell ETA receptors responsible for constriction.Key words: endothelium, endothelin, vein, artery, BQ123.
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Dissertations / Theses on the topic "Endothelium"

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Adner, Mikael. "Altered expression of contractile endothelin receptors in the vascular bed." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39103326.html.

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Kladakis, Stephanie M. "The role of proliferation and migration in endothelial cell monolayer formation on a tissue engineered blood vessel wall model." Diss., Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/16752.

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Wiseman, D. M. "The vascular endothelium : Angiogenesis and lymphocyte-endothelial cell interactions." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374797.

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Zhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.

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Thesis (M.S.)--West Virginia University, 2010.
Title from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).
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Tidwell, Caren Diana. "Endothelial cell interactions with model surfaces : effect of surface chemistry, surface mobility, and the adsorbed protein layer /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8004.

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Holmén, Carolina. "Mechanisms of endothelial cell dysfunction in Wegener's granulomatosis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-443-0/.

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Chauhan, Sharmila Deepa. "Mechanisms of endothelium-dependant dilation : a study of EDHF and endothelial dysfunction." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397184.

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TOPOUZIS, STAVROS. "Etudes in vitro des effets de facteurs endotheliaux sur la contraction du muscle lisse vasculaire." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR13190.

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L'endothelium vasculaire produit et libere plusieurs agents vasoactifs, comme le facteur relaxant endothelial (edrf) et le peptide vasocontracturant endotheline-1 (et-1). Le cotransport membranaire na#+-k#+-cl#- semble implique dans le processus de liberation de l'edrf par l'aorte isolee de rat, puisque le diuretique muzolimine, un inhibiteur de ce cotransport, inhibe selectivement les reponses relaxantes dependant de l'integrite de l'endothelium et dues a l'edrf. On considere que l'edrf agit en augmentant le taux tissulaire de gmp cyclique (gmpc). Dans l'aorte de rat, le 8-br gmpc peut produire une inhibition des contractions induites par les agonistes alpha-adrenergiques semblable a celle induite par l'endothelium. L'efficacite d'un agoniste determine l'amplitude de cette inhibition. Il y a une absence de correlation entre les augmentations du taux de gmpc et l'inhibition en resultant. L'et-1 et ses analogues structuraux, la sarafotoxine s6b, l'ala#3,11et-1 et l'ala#1,15et-1, induisent des contractions de l'aorte isolee de rat qui dependent en partie du calcium extracellulaire. Ces peptides ne semblent pourtant pas activer directement les canaux sensibles aux dihydropyridines. La presence de l'endothelium peut modifier seulement les contractions dues a l'et-1. Les differences fonctionnelles entre l'et-1 et ses analogues suggerent l'existence de sites d'action diverses ou de recepteurs differents pour ces peptides dans l'aorte de rat
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Mbanya, Dora Ngum Shu epouse. "The endothelium and hypercoagulability." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287138.

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Böhm, Felix. "The importance of endothelin-1 for vascular function in patients with atherosclerosis and healthy controls /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-293-0.

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Books on the topic "Endothelium"

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International Symposium on Endothelium-Derived Vasoactive Factors (1st 1989 Philadelphia, Pa.). Endothelium-derived contracting factors. Edited by Rubanyi Gabor M. 1947-, Vanhoutte Paul M, and International Symposium on Endothelium-Derived Vasoactive Factors (1st : 1989 : Philadelphia, Pa.). Basel: Karger, 1990.

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Catravas, John D., Allan D. Callow, and Una S. Ryan, eds. Vascular Endothelium. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8.

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Catravas, John D., Allan D. Callow, and Una S. Ryan, eds. Vascular Endothelium. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2437-3.

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Catravas, John D., C. Norman Gillis, and Una S. Ryan, eds. Vascular Endothelium. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8532-5.

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Catravas, John D., Allan D. Callow, C. Norman Gillis, and Una S. Ryan, eds. Vascular Endothelium. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6.

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Catravas, John D., Allan D. Callow, and Una S. Ryan, eds. Vascular Endothelium. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0.

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Voelkel, Norbert F., and Sharon Rounds, eds. The Pulmonary Endothelium. Chichester, UK: John Wiley & Sons, Ltd, 2009. http://dx.doi.org/10.1002/9780470747490.

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Salvador, Moncada, and Higgs Annie, eds. The vascular endothelium. Berlin: Springer, 2006.

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International Symposium on Endothelium-Derived Hyperpolarizing Factor (2nd 1998 Cernay-la-Ville, France). Endothelium-dependent hyperpolarizations. Amsterdam: Harwood Academic, 1999.

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F, Voelkel Norbert, and Rounds Sharon 1946-, eds. The pulmonary endothelium. Chichester, West Sussex: John Wiley & Sons, 2009.

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Book chapters on the topic "Endothelium"

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Carreras, Enric, M. Diaz-Ricart, S. Jodele, O. Penack, and S. Vasu. "Early Complications of Endothelial Origin." In The EBMT Handbook, 373–83. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_42.

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AbstractDuring HCT, the vascular endothelium is affected by conditioning, IS agents, inflammatory molecules released by injured cells and tissues, endotoxins translocated across injured mucosal barriers, the complex process of engraftment, and in allo-HCT immune alloreactivity. This endothelial damage can affect the entire vascular endothelium or that of specific organs and be the triggering event for several of the early complications grouped under denomination vascular endothelial syndromes of HCT.
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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Endothelium." In Encyclopedia of Exercise Medicine in Health and Disease, 282–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2335.

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Kwon, Sangmo, and Takayuki Asahara. "Endothelium." In Human Adult Stem Cells, 73–89. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2269-1_3.

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Brigham, Kenneth L. "The Clinical Profile of Sepsis and the Adult Respiratory Distress Syndrome." In Vascular Endothelium, 3–11. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_1.

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Gordon, John L. "Purine Regulation of Endothelial Cells: Relevance to Pathophysiology." In Vascular Endothelium, 111–16. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_10.

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Pearson, Jeremy D. "Autoantibodies to Endothelial Cells." In Vascular Endothelium, 117–25. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_11.

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Varani, James. "Leukocyte-Endothelial Cell Interactions." In Vascular Endothelium, 127–35. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_12.

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Lüscher, Thomas F., and Z. Yang. "Endothelium Function in Human Coronary Bypass Grafts." In Vascular Endothelium, 139–55. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_13.

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Perico, N., C. Zoja, and Giuseppe Remuzzi. "Altered Renovascular Endothelial Functions During Nephrotoxicity." In Vascular Endothelium, 157–66. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_14.

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Heistad, Donald D., F. Faraci, and G. Baumbach. "Cerebral Endothelial Function: Physiology and Pathophysiology." In Vascular Endothelium, 167–73. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3736-6_15.

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Conference papers on the topic "Endothelium"

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Swedenborg, J., S. Frebelius, S. Nydahl, and P. Olsson. "ROLE OF ANTITHROMBIN FOR INACTIVATION OF THROMBIN ON ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643342.

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Inactivation of thrombin which occurs mainly on the endothelium requires binding of the enzyme to receptors on the endothelial cells. One receptor for thrombin is glycosaminoglycans (GAG). Antithrombin (AT), however, also binds to GAG and may be involved in endothelial inactivation of thrombin.The purpose of the present study was to study the role of AT for the inhibition of thrombin on endothelium. The experiments were performed on rabbit aorta segment in vitro. Thrombin in solution and on the endothelial surface was functionally assayed with aid of a synthetic chromogenic substrate (thrombinS) or fibrinogen (thrombinF). In the latter case liberation of fibrinopeptide A (FPA) was measured. Inactivation of thrombin was estimated by the difference between loss of thrombin from the solution and recovery of thrombin on the endothelial surface during the incubation with thrombin.Preincubation of the endothelium with AT or plasma increased the inactivation of both thrombinS and thrombinF but AT-free plasma had no such effect. Preincubation with heparin (5 IU ml) decreas-the inactivation of thrombin on the endothelium. Endothelial segments preincubated with AT caused a much more rapid inactivation of thrombin over time as compared to control segments. Aortic segments preincubated with heparin caused a slower inactivation of thrombin on the sruface as compared to control segments.It is concluded, that preincubation with AT enhances the inactivation of thrombin on the endothelium whereas preincubation with heparin has the opposite effect. Heparin causes liberation of endogenous AT from the endothelial surface which may explain the decreased inactivation on the surface in the latter case.
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Stern, David M., Sara Rimon, Todd Scott, and Peter P. Nawroth. "MODULATION OF ENDOTHELIAL CELL COAGULANT PROPERTIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642946.

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As the cells forming the luminal vascular surface, endothelium is strategically located to play a role in the regulation of coagulation. Participation of endothelium in coagulation involves specific receptors on the cell surface functioning at the level of initiation and propagation of hemostatic reactions. In the anticoagulant protein C pathway, for example, the receptor thrombomodulin initiates thrombin-mediated activation of protein C and a binding site for protein S on bovine endothelium promotes assembly of the functional activated protein C/protein S complex. Endothelium also synthesizes, stores and releases functional protein S constitutively and in response to specific stimuli such as norepinephrine.Since activation of protein C requires thrombin formation in proximity to the vessel wall, we have examined procoagulant reactions on the endothelial cell surface. Endothelium provides a receptor for Factor IX/IXa which is relatively selective for the enzyme form and facilitates Factor IXa-VIII-mediated activation of Factor X. Half-maximal Factor Xa formation occurs at a Factor IXa concentration of 0.4nM on endothelium, whereas lOnM is required on liposomes. This concentration of Factor IXa corresponds to that which results in half-maximal occupancy of endothelial cell Factor IXa binding sites in the presence of Factors VIII and X, thus correlating kinetics and binding measurements. Crosslinking and ligand blotting studies have shown that the receptor is a protein with a molecular weight of ∼160,000. The clinical significance of this receptor is suggested by the moderately severe bleeding disorder observed in a patient with hemophilia B due to an abnormal Factor IX molecule, Factor IXalabama (Factor IXala). Although the coagulant activity of Factor IXala is only mildly decreased on phospholipids, it is severely impaired on endothelium. The affinity of Factor IXala for the endothelial cell Factor X activation complex is decreased by 20-fold compared with the normal enzyme and the binding affinity is similarly decreased. Since the molecular defect in Factor IXala has been previously shown to consist of a single point mutation in the growth factor domain, this indicates a role for the growth factor domain in receptor, recognition.The picture of endothelial cell coagulant properties which emerges from these and other studies is one in which endothelium has either an anticoagulant or procoagulant potential, depending on modulation of receptor expression and release of secreted products. In the quiescent state, anticoagulant mechanisms predominate with only limited amounts of procoagulant activity: there is little tissue factor activity and only a basal level of receptors for Factor IX/lXa. Activation of endothelium by Tumor Necrosis Factor (TNF) or Interleukin 1 can shift this balance. Tissue factor synthesis and expression occurs in a dose-dependent manner, being half-maximal at a TNF concentration of about 150pM. TNF also increases the number of Factor IX/lXa binding sites. Concomitant with enhancement of endothelial cell procoagulant properties is a suppression of cell surface cofactor activity for the anticoagulant protein C pathway. Endothelial cell-dependent, thrombin-mediated activated protein C formation is decreased by 70-80% and activated protein C-protein S-mediated Factor Va inactivation decreases by over 90%. Following the in vivo infusion of Interleukin 1, similar changes in endothelial cell coagulant properties were observed on aortic segments with fibrin deposition occurring on the functionally altered, but morphologically intact endothelium. This modulation of endothelial cell coagulant properties could underlie the prothrombotic state associated with inflammatory disorders and could also explain the recently observed selective intravascular thrombosis of tumor vasculature seen in vivo in meth A sarcomas after administration of TNF.Thus, although endothelium was initially felt to be hemostatically inert, this apparent lack of activity actually masks a delicate balance of procoagulant and anticoagulant mechanisms. The balance can be effectively shifted by physiologic mediators, such as monokines, which alter receptor expression on the endothelial cell surface. Changes in endothelial cell hemostatic properties may be an early indicator of vessel wall disease and underlie the pathogenesis of localized thrombotic processes.
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Vanhoutte, Paul M. "PLATELETS, ENDOTHELIUM AND VASOSPASM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643722.

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The endothelium can secrete both relaxing and contracting substances. One of the most powerful stimuli to the release of the former are thrombin and aggregating platelets. This contributes to the protective role of the endothelium against inappropriate intraluminal platelet aggregation and coagulation in blood vessels with an intact intima. Thrombin-induced, endothelium-dependent relaxations have been obtained in isolated arteries of different species, including humans. Endothelium-dependent relaxations can be evoked by autologous platelets in isolated blood vessels of the dog, pig and rat; they can be obtained in canine coronary arteries with human platelets. The major platelet-products involved in these endothelium-dependent relaxations are 5-hydroxytryptamine (serotonin) and the adenine nucleotides. Although platelet-activating factor (PAF) can evoke endothelium-dependent relaxation it only does so at concentrations much higher than those occurring under physiological conditions; since the relaxations are not prevented by PAF-antagonists, they are non-specific in nature.The receptor mediating the endothelium-dependent relaxations to serotonin released from the aggregating platelets can be subtyped as a S1~(5HT1) serotonergic receptor;those mediating the response to the adenine nucleotides as P2y-purinergic receptors. In the absence of the endothelium aggregating platelets cause contractions of vascular smooth muscle; these are mediated by a mixture of S1-like and S2~serotoner-gic receptors in coronary arteriesof the dog, and by S2-serotonergic receptors in those of the pig. Thus, in the porcine coronary artery, the S2-serotonergic antagonist ketanserin markedly enhances the platelet-induced endothelium-dependent relaxation. After previous (four weeks) injury, the regenerated endothelium of the porcine coronary artery loses the ability to respond to serotonin,and is unable to prevent the constrictionsevoked by aggregating platelets. The endothelium-dependent relaxations of porcine coronary arteries evoked by aggregating platelets are potentiated by chronic treatmentof the donor animals with cod liver oil. These studies emphasize the protective roleof the endothelial cells against the vasoconstriction (vasospasm) induced by aggregating platelets. This role is depressed after previous injury, and can be facilitatedby dietary adj ustments.
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Nawroth, Peter P., Jerry Brett, Susan Steinberg, Charles T. Esmon, and David M. Stern. "ENDOTHELIUM AND PROTEIN S: SYNTHESIS, RELEASE AND REGULATION OF ANTICOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642962.

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The protein C-protein S pathway is closely linked to the vessel wall. In terms of protein C, endothelium has been shown to provide the receptor thrombomodulin, which promotes thrombin-mediated formation of activated protein C. Optimal anticoagulant function of activated protein C requires protein S and a cellular surface. Recent studies have indicated that endothelium can facilitate assembly of the activated protein C-protein S complex and that bovine endothelium expresses specific binding site(s) for protein S which promote its anticoagulant function. Expression of protein S binding sites is subject to down-regulation by Tumor Necrosis Factor (TNF) . Exposure of cultured bovine endothelium to TNF results in decreased 125I-protein s binding and attenuated rates of Factor Va inactivation after 2 hrs followed by negligible 125I-protein S binding and Factor Va inactivation by 10 hrs. These changes persist for over 48 hrs, in contrast to the more transient rise in endothelial cell tissue factor induced by TNF which returns to baseline by 24 hrs.In addition to providing binding sites for protein S, endothelium constitutively synthesizes and releases this vitamin K-dependent anticoagulant cofactor. Release of protein S is blocked by addition of warfarin, indicating that y-carboxylation facilitates the release of intracellular protein S. Morphologic studies, at the level of electron microscope, have shown protein S antigen to be present in cisternae of rough endoplasmic reticulum, the trans face of the golgi and a population of intracellular vesicles which appear to be distributed at the cellular periphery. By immunofluorescence, the distribution of protein S is distinct from that of von Willebrand Factor. The intracellular vesicles containing protein S constitute a storage pool potentially available for rapid release. Treatment of endothelium with norepinephrine results in release of protein S over the next 20 min. Release is half-maximal at a norepinephrine concentration of about 0.1 uM and is not observed with the biologically inactive entantiomer (+) norepinephrine. Norepinephrine-induced release of intracellular protein S can be blocked by prazosine (10-7 7 M), but not by propranolol (10-6 M) or yohimbine (10-5 M). These data are consistent with release of protein S being a receptor-mediated process dependent on an endothelial cell alpha 1 adrenergic receptor. Blockade of norepinephrine-induced release of protein S by pertussis toxin treatment of endothelium further defines the intracellular pathway of protein S and implicates regulatory G proteins in the stimulus-response coupling. Electron microscopic studies have shown that following exposure of endothelium to norepinephrine the intracellular vesicles containing protein S undergo exocytosis at the plasma membrane. These data define a new relationship between the autonomic nervous system and the coagulation mechanism.Protein S is clearly an endothelial cell-associated anticoagulant protein. A specific binding site on the endothelial cell surface can regulate its anticoagulant function on the vessel wall. Endothelial cell synthesis and release of protein S defines a new level of participation of endothelium in the protein C-protein S pathway.
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van Wamel, Annemieke. "Microbubbles Reforming Endothelium." In THERAPEUTIC ULTRASOUND: 5th International Symposium on Therapeutic Ultrasound. AIP, 2006. http://dx.doi.org/10.1063/1.2205431.

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Lei, Xiaoxiao, Michael B. Lawrence, and Cheng Dong. "Mechanics of Cell Rolling Adhesion in Shear Flow." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0284.

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Abstract Leukocyte rolling along endothelial cells is a critical step of leukocyte-endothelium interaction, which plays important roles in tissue inflammation and wound healing [1]. The occurrence of rolling results from the dynamic balance of hemodynamic shearing force acting on the cell and adhesive bond force between cell and endothelium, while the balance strongly depends on the leukocyte deformability [2]. The objective of this study is to elucidate the effects of (1) hydrodynamic shear stress, (2) cell deformation, and (3) surface adhesion strength on the rolling adhesion event through in vitro experiment and theoretical simulation.
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Dai, Z., B. Liu, D. Yi, X. Xia, K. Ramirez, R. Dong, A. Gao, V. Kalinichenko, and M. Fallon. "Lung Capillary Endothelium to Arterial Endothelium Transition in Pulmonary Arterial Hypertension." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4697.

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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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Görög, P., and V. V. Kakkar. "INCREASED UPTAKE OF MONOCYTE-TREATED LOW-DENSITY LIPOPROTEINS BY AORTIC ENDOTHELIUM IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643356.

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A new technique was elaborated for measuring LDL uptake by rat aortic endothelial cells in vivo, using a fluorescent marker (Dil)-labelled LDL and quantifying the fluorescence in cells selectively removed from the aorta. This technique was used to study the endothelial uptake of LDL modified by activated human monocytes (LDL-A) in comparison with native LDL (LDL-N) protected from oxidation by vitamin E during the preparation. Incubation of LDL with activated monocytes increased endothelial uptake in vivo by 9.3-fold (from 410 ± 99 to 3803 ± 580, ng LDL/106 cells, mean ± s.e.m., p < 0.001) and also by a 4.4-fold (from 613 ± 217 to 2718 ± 605, ng LDL/106 cells, p < 0.01) in cultured confluent porcine endothelium. In contrast, only a 1.5-fold increase (p < 0.05) in uptake of LDL-A was observed in sparse cultures. Cytotoxicity of monocyte-altered or native LDL did not differ as measured by the [3H] deoxyglucose-release test on cultured endothelium. Our results suggest that modification of LDL in the circulation by monocytes may make an important contribution to atherogenesis.
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Shatos, M., J. Doherty, D. Allen, and J. Hoak. "ALTERATIONS IN VASCULAR ENDOTHELIAL CELL FUNCTION BY OXYGEN-FREE RADICALS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643365.

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The vascular endothelium is a target for oxidant-induced damage in many disease states including hyperoxia, inflammation, ischemia and reperfusion injury. However, little is known concerning oxidant injury to endothelial cells and its relationship to hemostasis. Our studies have focused on the ability of oxygen free radicals to injure and/or alter selected vascular endothelial cell functions pertinent to the regulation of hemostasis. Xanthine and xanthine oxidase, a well-characterized generating system for the production of the superoxide anion radical (O− 2) was used to sublethally injure human umbilical vein endothelial cells (HUVE) in vitro. We examined the effects of a 15 min exposure of HUVE cells to xanthine (50μM), and xanthine oxidase (2.5-100mU) (previously determined to be non-toxic using trypan blue dye exclusion) on platelet adherence, and prostacyclin release using established assays. The antioxidant enzymes superoxide dismutase (SOD) 200μg/ml and catalase 50μg/ml were added to endothelium incubation systems to evaluate any protective effects upon O− 2-induced alterations. All experiments were conducted in a serum-free HEPES-Tyrode's buffer, pH 7.4 incubation system. Our results show that exposure of HUVE cells to sublethal concentrations of oxygen free radical generating systems causes significant enhancement of platelet adherence (65%) to injured endothelium. A 12-fold increase in prostacyclin release resulted after a 15 min treatment with xanthine and xanthine oxidase. The addition of exogenous PGI2 (150nM) to platelet-endothelial systems did not completely prevent the enhanced platelet adherence suggesting that lack of prostacyclin was not completely responsible for the adherence of platelets to O− 2 injured cells. When SOD and catalase, scavengers of O− 2 and H2O− 2, were added to treated cells, platelet adherence decreased by 42-77% and prostacyclin release approached that of control cultures. These data implicate an active participation of activated metabolites of molecular oxygen in the alteration of vascular endothelial cell function.
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Reports on the topic "Endothelium"

1

Klauber-DeMore, Nancy. Characterization of Gene Expression in Human Breast Tumor Endothelium. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada486849.

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2

Lu, Bo. Radiation Sensitization Via Inhibiting Survival of Prostate Cancer and its Vascular Endothelium. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada473670.

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Matthew, Candace B., Ingrid V. Sils, and Amy M. Bastille. Flunarizine Attenuates Hypothermia/Rewarming-Induced Changes in Protein and Water Movement Across the Endothelium of Rats. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada414632.

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Furbert-Harris, Paulette M. Eosinophil Cell Lines in a Tri-Cell Multicellular Tumor Spheroid (MTS)/Endothelium Complex: Down Regulation of Adhesion and Integrin Molecules-Implications of Metastasis Inhibition. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada442676.

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Nguyen Brooks, Mai H. Endothelial Genes. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439227.

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Gakhar, Gunjan. CTC-Endothelial Cell Interactions during Metastasis. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada609384.

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Gakhar, Gunjan. CTC-Endothelial Cell Interactions during Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580364.

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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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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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Al-Attar, Ali. Cell Surface Molecules Driving Breast Cancer/Endothelial Interactions. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396252.

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