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Endothelial Lining (endothelial + lining)
Selected AbstractsDexamethasone alters F-actin architecture and promotes cross-linked actin network formation in human trabecular meshwork tissueCYTOSKELETON, Issue 2 2005Abbot F. Clark Abstract Elevated intraocular pressure is an important risk factor for the development of glaucoma, a leading cause of irreversible blindness. This ocular hypertension is due to increased hydrodynamic resistance to the drainage of aqueous humor through specialized outflow tissues, including the trabecular meshwork (TM) and the endothelial lining of Schlemm's canal. We know that glucocorticoid therapy can cause increased outflow resistance and glaucoma in susceptible individuals, that the cytoskeleton helps regulate aqueous outflow resistance, and that glucocorticoid treatment alters the actin cytoskeleton of cultured TM cells. Our purpose was to characterize the actin cytoskeleton of cells in outflow pathway tissues in situ, to characterize changes in the cytoskeleton due to dexamethasone treatment in situ, and to compare these with changes observed in cell culture. Human ocular anterior segments were perfused with or without 10,7 M dexamethasone, and F-actin architecture was investigated by confocal laser scanning microscopy. We found that outflow pathway cells contained stress fibers, peripheral actin staining, and occasional actin "tangles." Dexamethasone treatment caused elevated IOP in several eyes and increased overall actin staining, with more actin tangles and the formation of cross-linked actin networks (CLANs). The actin architecture in TM tissues was remarkably similar to that seen in cultured TM cells. Although CLANs have been reported previously in cultured cells, this is the first report of CLANs in tissue. These cytoskeletal changes may be associated with increased aqueous humor outflow resistance after ocular glucocorticoid treatment. Cell Motil. Cytoskeleton 60:83,95, 2005. © 2004 Wiley-Liss, Inc. [source] The origin of the endothelial cells: an evo-devo approach for the invertebrate/vertebrate transition of the circulatory systemEVOLUTION AND DEVELOPMENT, Issue 4 2005R. Muñoz-Chápuli Summary Circulatory systems of vertebrate and invertebrate metazoans are very different. Large vessels of invertebrates are constituted of spaces and lacunae located between the basement membranes of endodermal and mesodermal epithelia, and they lack an endothelial lining. Myoepithelial differentation of the coelomic cells covering hemal spaces is a frequent event, and myoepithelial cells often form microvessels in some large invertebrates. There is no phylogenetic theory about the origin of the endothelial cells in vertebrates. We herein propose that endothelial cells originated from a type of specialized blood cells, called amoebocytes, that adhere to the vascular basement membrane. The transition between amoebocytes and endothelium involved the acquisition of an epithelial phenotype. We suggest that immunological cooperation was the earliest function of these protoendothelial cells. Furthermore, their ability to transiently recover the migratory, invasive phenotype of amoebocytes (i.e., the angiogenic phenotype) allowed for vascular growth from the original visceral areas to the well-developed somatic areas of vertebrates (especially the tail, head, and neural tube). We also hypothesize that pericytes and smooth muscle cells derived from myoepithelial cells detached from the coelomic lining. As the origin of blood cells in invertebrates is probably coelomic, our hypothesis relates the origin of all the elements of the circulatory system with the coelomic wall. We have collected from the literature a number of comparative and developmental data supporting our hypothesis, for example the localization of the vascular endothelial growth factor receptor-2 ortholog in hemocytes of Drosophila or the fact that circulating progenitors can differentiate into endothelial cells even in adult vertebrates. [source] Possible role of exogenous cAMP to improve vascular endothelial dysfunction in hypertensive ratsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2006Dhvanit I. Shah Abstract The study has been designed to investigate the effect of 8-Br-cAMP, an activator of protein kinase A, in hypertension-induced vascular endothelial dysfunction. Rats were uninephroctomized and desoxycortisone acetate (DOCA) (40 mg/kg, s.c.) was administered to rats to produce hypertension (mean arterial blood pressure > 140 mmHg). Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, electron microscopy of thoracic aorta and serum concentration of nitrite/nitrate. The expression of mRNA for p22phox and eNOS was assessed by using reverse transcriptase-polymerase chain reaction. Serum thiobarbituric acid reactive substances concentration and aortic superoxide anion concentration were estimated to assess oxidative stress. 8-Br-cAMP (5 mg/kg, i.p.) or atorvastatin (30 mg/kg, p.o.) prevented hypertension-induced attenuation of acetylcholine-induced endothelium-dependent relaxation, impairment of vascular endothelial lining, decrease in expression of mRNA for endothelial nitric oxide synthase (eNOS), serum nitrite/nitrate concentration and increase in expression of mRNA for p22phox, superoxide anion and serum TBARS. The ameliorative effect of 8-Br-cAMP was prevented by N -nitro- l -arginine methyl ester (25 mg/kg, i.p.) and glibenclamide (30 mg/kg, i.p.). It may be concluded that 8-Br-cAMP may stimulate expression and activity of eNOS and suppress expression of p22phox subunit of NADPH oxidase to reduce oxidative stress and subsequently improve vascular endothelial dysfunction. [source] CC531S-induced damage of the rat liver sinusoidal endothelial lining is mediated by the Fas/FasL pathwayHEPATOLOGY, Issue 5 2003Katrien Vekemans No abstract is available for this article. [source] The Immunological Hurdles to Cardiac XenotransplantationJOURNAL OF CARDIAC SURGERY, Issue 6 2001Jeffrey L. Platt M.D. ABSTRACT The main hurdle to clinical application of cardiac xenotransplantation is the immune response of the recipient against the graft. Although all xenografts arouse an intense immune response, the effect of that response depends very much on whether the graft consists of isolated cells or an intact organ, such as the heart. Intact organs, which are transplanted by primary vascular anastomosis, are subject to severe vascular injury owing to the reaction of immune elements with the endothelial lining of donor blood vessels. Vascular injury leads to hyperacute rejection, acute vascular rejection, and chronic rejection. The immunological basis for these types of rejection and potential therapies, which might be used to avert them, are discussed. [source] Blood,brain barrier efflux transportJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 9 2003Pamela L. Golden Abstract Efflux transport at the blood,brain barrier (BBB) limits the brain tissue exposure to a variety of potential therapeutic agents, including compounds that are relatively lipophilic and would be predicted to permeate the endothelial lining of the brain microvasculature. Recent advances in molecular and cell biology have led to identification of several specific transport systems at the blood,brain interface. Refinement of classical pharmacokinetic experimentation has allowed assessment of the structural specificity of transporters, the impact of efflux transport on brain tissue exposure, and the potential for drug,drug interactions at the level of BBB efflux transport. The objective of this minireview is to summarize efflux transporter characteristics (location, specificity, and potential inhibition) for transport systems identified in the BBB. A variety of experimental approaches available to ascertain or predict the impact of efflux transport on net brain tissue uptake of substrates also are presented. The potential impact of efflux transport on the pharmacodynamics of agents acting in the central nervous system are illustrated. Finally, general issues regarding the role of identifying efflux transport as part of the drug development process are discussed. © 2003 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 92:1739,1753, 2003 [source] CC531s colon carcinoma cells induce apoptosis in rat hepatic endothelial cells by the Fas/FasL-mediated pathwayLIVER INTERNATIONAL, Issue 4 2003Katrien Vekemans Abstract The mechanisms involved in colorectal carcinoma with liver metastasis are not well known. Metastasizing colon carcinoma cells express more FasL than primary colon carcinoma cells and cancer cells induce apoptosis in hepatocytes by the Fas/FasL pathway. Therefore, this study focused on Fas/FasL expression and functionality in rat liver sinusoidal endothelial cells (LSECs) and CC531s colon carcinoma cells in vitro and in vivo. RT-PCR and immunochemistry revealed Fas and FasL in LSECs and CC531s, respectively. Functionality of Fas was assessed in vitro by incubation with human recombinant FasL (1,100 ng/ml) with or without enhancer. At concentrations of 10 and 100 ng/ml with enhancer, respectively 21% and 44% of endothelial cells showed signs of apoptosis using Hoechst 33342/propidium iodide staining and electron microscopy. In co-cultures, apoptosis could be detected in endothelial cells neighboring the CC531s and could be inhibited by an antagonistic FasL antibody. Moreover, 18 h after mesenteric injection of CC531s, the sinusoidal endothelium revealed disruption. In conclusion, (i) CC531s cells induce apoptosis in LSECs in vitro by using Fas/FasL; (ii) CC531s cells damage the sinusoidal endothelial lining in vivo; and (iii) this might provide FasL-positive tumor cells a gateway towards the hepatocytes. [source] Dermoscopic findings of haemosiderotic and aneurysmal dermatofibroma: report of six patientsBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2006P. Zaballos Summary Background, The clinical diagnosis of dermatofibroma is commonly easy. However, the differentiation of dermatofibroma from other cutaneous tumours is difficult in some instances, primarily in atypical cases and rare variants. Haemosiderotic dermatofibroma is a variant composed of numerous small vessels, extravasated erythrocytes and intra- and extracellular haemosiderin deposits. Aneurysmal dermatofibroma is a variant composed of large, blood-filled spaces without endothelial lining. Some authors consider that haemosiderotic dermatofibroma is an early stage in the development of aneurysmal dermatofibroma. The clinical differential diagnosis of haemosiderotic or aneurysmal dermatofibroma must include melanoma and other melanocytic tumours, vascular neoplasms, adnexal tumours and nonspecific cysts. Dermoscopy improves the diagnostic accuracy in pigmented and nonpigmented skin lesions. Objectives, To evaluate specific dermoscopic criteria. Methods, Dermoscopic examination (using the DermLite Foto; 3Gen, LLC, Dana Point, CA, U.S.A.) of six patients with haemosiderotic or aneurysmal dermatofibromas was performed to evaluate specific dermoscopic criteria. Results, A multicomponent pattern with a central bluish or reddish homogeneous area in combination with white structures and a peripheral delicate pigment network along with vascular structures was noted in five of six lesions. Conclusions, This dermoscopic pattern yielded the diagnosis of haemosiderotic or aneurysmal dermatofibroma in most cases. However, this multicomponent pattern may present in some melanomas and although it is useful in determining a clinical diagnosis of aneurysmal dermatofibroma, it may not be specific to this entity. [source] | |||||||||||||