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  1. Home
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Browsing by Subject "Endothelial cell"

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    Angiogenesis and the role of bone marrow endothelial cells in haematological malignancies
    (Murcia : F. Hernández, 2004) De Raeve, H.; Van Marck, E.; Van Camp, B.; Vanderkerken, K.
    Increased microvessel density (MVD) has been observed in the bone marrow (BM) of patients with multiple myeloma (MM), acute lymphoblastic leukaemia, acute myeloid leukaemia, and myelodysplastic and myeloproliferative syndrome. The MVD is the net result of cumulative phases of angiogenesis and angio-regression and is as such not an indicator of the ongoing angiogenesis at the time of biopsy. There is, therefore, a need for additional methods that allow the estimation of ongoing angiogenesis. Double immunostainings for CD34 and Ki-67 can be used on paraffin-embedded tissue to determine the endothelial proliferation fraction. The BM endothelial cells, as a component of the BM stroma, have a close interaction with the malignant cells. In MM, for example, they are involved in the specific homing and are a source of paracrine growth factors. Targeting the BM microvessels will not only influence the nutrient and oxygen supply, but will in addition reduce the growth stimuli provided by the EC.
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    Blood-borne cells involved in arterial repair upon experimental incision injury
    (Murcia : F. Hernández, 2008) Pieri, L.; Rinaldi, B; Domenici Lombardo, L.; Bacci, S.; Filippelli, A.; Capuano, A.; Rossi, F.; Romagnoli, P.
    Summary. We had previously shown that microscopically detectable infiltration of dendritic cells and expression of Hsp47 in tissue lysates occur during repair upon experimental arterial injury. We have further analysed here the cell types involved in the repair process by histology, electron microscopy and immunofluorescence. Rat carotid arteries were subjected to brief crushing and full thickness incision and were analysed up to 21 d thereafter. Adhesion and activation of platelets occurred 3 h after surgery. A neointima had formed 7 d after surgery, where immature cells entered from the lumen and gave rise to cells rich in organelles of the secretory pathway and endowed with bundles of phalloidin-binding microfilaments. Alpha smooth muscle-positive, secretory and contractile smooth muscle cells were found in the neointima 14 and 21 d after injury. Seven to 21 d after surgery, endothelial cells appeared immature and the newly formed tissue contained MHC-II positive, CD43 positive dendritic cells which clustered with lymphocytes, a few macrophages containing apoptotic remnants and cells labelled for Hsp47. Thin elastic fibrils appeared in the neointima 21 d after injury. The results suggest that the response to acute arterial incision injury is mediated by blood borne cells which differentiate along multiple pathways; the process evolves without reaching stabilization within the observed time lapse; the secretion of extracellular matrix is marked by the expression of Hsp47; and the constant presence of dendritic cells clustered with lymphocytes makes these cells candidate to a pivotal role in the tissue response to injury.
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    Crosstalk between endothelial cell and thrombus in chronic thromboembolic pulmonary hypertension: perspective
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Sakao, Seiichiro; Tatsumi, Koichiro
    It is generally accepted that chronic thromboembolic pulmonary hypertension (CTEPH) results from pulmonary emboli originating from deep vein thrombosis. However, this consensus opinion has been challenged, and the concept that some aspects of CTEPH exacerbation might result from a small-vessel disease leading to secondary thrombosis has been suggested. In addition to the effect of recurrent thromboembolism, a number of lines of clinical evidence indicate that progressive worsening is contributed to by remodeling in the small pulmonary arteries. Histopathological studies of the microvascular changes in CTEPH have identified vascular lesions similar to those seen in idiopathic pulmonary arterial hypertension (IPAH). Especially in in vitro and ex vivo experiments, pulmonary artery endothelial cells (ECs) in pulmonary hypertensive diseases are suggested to exhibit an unusual hyperproliferative potential with decreased susceptibility to apoptosis, indicating that dysfunctional ECs may contribute to the progression of the diseases. Although the degree and mechanisms of EC dysfunction as a contributor to CTEPH are unclear, EC dysfunction may occur in small arteries. Indeed, the cells stimulated by the microenvironment created by the unresolved clot may release substances that induce EC dysfunction. The EC dysfunctions in CTEPH may lead to disorders of the anti-coagulation properties in ECs and may result in additional clots in situ. Moreover, these may lead to the progression, not only of distal thrombus, but also of proximal clotting. This article reviews the pathobiological concepts of CTEPH and explains a crosstalk between EC dysfunction and in situ thrombi which may contribute to the vascular lesions of CTEPH.
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    Evaluation of microvascular density in tumors, pro and contra
    (Murcia : F. Hernández, 2008) Nico, Beatrice; Benagiano, Vicenzo; Mangieri, Doménica; Maruotti, Nicola; Vacca, Angelo; Ribatti, Doménico
    Microvascular density (MVD) counting protocols have become the morphological gold standard to assess the neovasculature in human tumors. This method requires the use of specific markers to vascular endothelium and of immunohistochemical procedures to visualize microvessels. MVD determined in primary tumors is significantly associated with metastasis and prognosis in several tumors and is most predictive in those tumors that induce significant angiogenesis, namely carcinomas of breast and prostate, and haematological malignancies. There is such a wide range of antibodies and suppliers, antigen retrieval methods, designation of high and low vessel count groups, patient study groups and data interpretation, that it is exceedingly difficult to compare results.
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    Intimal thickening in arterial autografts. Role of the adventitial layer
    (Murcia : F. Hernández, 1992) Buján, J.; Bellón, J.M.; Gianonatti, M.C.; Golitsin, A.
    In the present work, the repairing response of the iliac arterial wall is studied after carrying out autografts in segments of these vessels. The formation of the intimal hyperplasia, which occurred in al1 the cases, was followed at the biochemical leve1 (tritium thymidine incorporation) and with light and electron microscopy. The adventitial layer showed great activity during the repairing process. We believe that it plays an important role not only in neoadventitial formation, but also in myointimal raising.
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    Ontogeny of reactivity to endothelial cell markers during development of the embryonic and fetal rat lung
    (Murcia : F. Hernández, 1992) Han, R.N.N.; Tanswell, A.K.; Post, M.
    The reactivity of endothelial cells to putative endothelial cell-specific markers varies with species,with vessel size and with the organ studied. To determine their value in studies of fetal rat lung, and whether organ immaturity would also influence reactivity, we studied endothelial cell immunoreactivity to antibodies against Factor VIIIIvon Willebrand factor (VIII/vWF), and binding reactivity to Bandeiraea (Griffonia) simplicifolia 1 lectin (BSL 1) during rat fetal lung development. Using an indirect immunofluorescent technique to detect Factor VIIYvon Willebrand factor (VIIUvWF), endothelial cells lining the aortic arches were identified as early as day 11 of gestation (term= 22 days), prior to lung development. Immunoreactivity to VIIIIvWF was subsequently localized to intrapulmonary endothelial cells and was not dependent on vessel size. In contrast, binding reactivity of FITC-conjugated BSL 1 was observed to both endothelial cells and to the basement membrane of developing airways, thus limiting its value as endothelial cell marker. During very early lung development solitary angioblasts could not be identified by reactivity to either VIIYvWF antibodies or to BSL 1, and neither marker appears to be of value for studies of early angiogenic events.
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    The role of the pericytes of the adventitial microcirculation in the arterial intimal thickening
    (Murcia : F. Hernández, 1990) Díaz-Flores, Lucio; Valladares, Francisco; Gutiérrez, Ricardo; Varela, Hilda
    Segments of rat femoral arteries, with one collateral each, occluded between ligatures and dissected from surrounding tissue, developed intimal thickening, with or without ligation of their collaterals. Numerous newly-formed capillaries from the surrounding arterial rnicrocirculation growing into the adventitia, tunica media and intimal thickening were demonstrated by means of serial longitudinal sections, predominantly in the ostium of the collateral. When the ligatures were applied without damaging the microcirculation surrounding the artery and the normal continuity of the adventitial vessels was unchanged, earlier presence of intimal thickening was observed. When the fibrous layers of the adventitia were removed at the moment of the arterial ligation, the continuity between newlyformed vessels of the neoadventitia and those growing into the media and neointima was much more evident. It was then noted that the pericytes constituted a major component of the intimal thickening. The introduction of contrast material in rnicrocirculation confirmed the connections between newly-formed adventitial and intimal vessels. At the beginning of the experiment, autoradiographic studies showed an increased DNA synthesis in the cells of preformed postcapillary venules and capillaries of surrounding arterial microcirculation and later in those of the newly-formed vessels growing into the arterial wall. These results indicate that newlyformed capillaries derived from surrounding arterial microcirculation penetrate the wall of the occluded arterial segments and contribute to the intimal thickening formation. It is likely that the pericytes and endothelial cells (EC) of these ingrowing vessels are sources of myointimal cells at the intimal thickening and of endothelium at the luminal surface, respectively.
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    Visualisation and stereological assessment of blood and lymphatic vessels
    (F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Lokmic, Zerina; Mitchell, Geraldine M.
    The physiological processes involved in tissue development and regeneration also include the parallel formation of blood and lymphatic vessel circulations which involves their growth, maturation and remodelling. Both vascular systems are also frequently involved in the development and progression of pathological conditions in tissues and organs. The blood vascular system circulates oxygenated blood and nutrients at appropriate physiological levels for tissue survival, and efficiently removes all waste products including carbon dioxide. This continuous network consists of the heart, aorta, arteries, arterioles, capillaries, post-capillary venules, venules, veins and vena cava. This system exists in an interstitial environment together with the lymphatic vascular system, including lymph nodes, which aids maintenance of body fluid balance and immune surveillance. To understand the process of vascular development, vascular network stability, remodelling and/or regression in any research model under any experimental conditions, it is necessary to clearly and unequivocally identify and quantify all elements of the vascular network. By utilising stereological methods in combination with cellular markers for different vascular cell components, it is possible to estimate parameters such as surface density and surface area of blood vessels, length density and length of blood vessels as well as absolute vascular volume. This review examines the current strategies used to visualise blood vessels and lymphatic vessels in two- and three-dimensions and the basic principles of vascular stereology used to quantify vascular network parameters.

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