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MeSH: adventicie

5 záznamů v Medvik Filtry

Článek

How many Layers has the Adventitia? - Structure of the Arterial Tunica Externa Revisited

Witter, K
Autor Witter, K Department of Pathobiology, Institute of Anatomy, Histology and Embryology, University of Veterinary Medicine Vienna, Veterinärplatz 1, 1210, Vienna, Austria
Tonar, Z
Autor Tonar, Z Department of Histology and Embryology and Biomedical Centre, Faculty of Medicine in Pilsen, Charles University in Prague, Karlovarská 48, 30166, Pilsen, Czech Republic
Schöpper, H
Autor Schöpper, H Department of Pathobiology, Institute of Anatomy, Histology and Embryology, University of Veterinary Medicine Vienna, Veterinärplatz 1, 1210, Vienna, Austria

Anatomia, Histologia, Embryologia. 2017 ; 46 (2) : 110-120. [pub] 20160610

Anat Histol Embryol
ISSN 1439-0264
Medvik
Zdroj

Tunica adventitia or tunica externa is the outer layer of the blood vessel wall. It consists of connective tissue with vasa and nervi vasorum and plays a key role in vascular health. The aim of our study was to compare the wall layers beyond tunica media in arteries of different type and location. The following arteries of pig, dog and cat were processed histologically and analysed by light microscopy: aorta ascendens, arcus aortae, aorta thoracica, aorta abdominalis, arteria (a.) femoralis, a. tibialis cranialis, a. carotis communis, a. lingualis, a. basilaris, a. cerebralis media, a. testicularis and aa. jejunales. We found two layers of connective tissue outside the media: (1) a compact layer with many elastic fibres in muscular and few in elastic arteries and (2) an outer layer of loose connective tissue. The compact layer was missing in aorta ascendens, arcus aortae and intracranial vessels. Adventitial stripping removed only the loose connective tissue layer. In spite of the still present compact layer, stripped arteries were very flimsy. We suggest using the term 'tunica externa' for the compact connective tissue layer and 'tunica adventitia' for the outermost loose connective tissue layer as in other organs. The presence of the tunica externa differs between species, arteries and arterial side, as well as the removability of tunica adventitia and tunica externa by anatomical dissection.

MeSH
adventicie anatomie a histologie MeSH
aorta abdominalis anatomie a histologie MeSH
aorta thoracica anatomie a histologie MeSH
elastická tkáň anatomie a histologie MeSH
kočky anatomie a histologie MeSH
prasata anatomie a histologie MeSH
psi anatomie a histologie MeSH
svaly hladké cévní anatomie a histologie MeSH
zvířata MeSH
Check Tag
kočky anatomie a histologie MeSH
psi anatomie a histologie MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH

Článek

Metabolic Reprogramming Regulates the Proliferative and Inflammatory Phenotype of Adventitial Fibroblasts in Pulmonary Hypertension Through the Transcriptional Corepressor C-Terminal Binding Protein-1

Circulation (New York, N.Y.). 2016 ; 134 (15) : 1105-1121. [pub] 20160825

Circulation (New York)
ISSN 1524-4539
Medvik
Zdroj

BACKGROUND: Changes in metabolism have been suggested to contribute to the aberrant phenotype of vascular wall cells, including fibroblasts, in pulmonary hypertension (PH). Here, we test the hypothesis that metabolic reprogramming to aerobic glycolysis is a critical adaptation of fibroblasts in the hypertensive vessel wall that drives proliferative and proinflammatory activation through a mechanism involving increased activity of the NADH-sensitive transcriptional corepressor C-terminal binding protein 1 (CtBP1). METHODS: RNA sequencing, quantitative polymerase chain reaction,(13)C-nuclear magnetic resonance, fluorescence-lifetime imaging, mass spectrometry-based metabolomics, and tracing experiments with U-(13)C-glucose were used to assess glycolytic reprogramming and to measure the NADH/NAD(+) ratio in bovine and human adventitial fibroblasts and mouse lung tissues. Immunohistochemistry was used to assess CtBP1 expression in the whole-lung tissues. CtBP1 siRNA and the pharmacological inhibitor 4-methylthio-2-oxobutyric acid (MTOB) were used to abrogate CtBP1 activity in cells and hypoxic mice. RESULTS: We found that adventitial fibroblasts from calves with severe hypoxia-induced PH and humans with idiopathic pulmonary arterial hypertension (PH-Fibs) displayed aerobic glycolysis when cultured under normoxia, accompanied by increased free NADH and NADH/NAD(+) ratios. Expression of the NADH sensor CtBP1 was increased in vivo and in vitro in fibroblasts within the pulmonary adventitia of humans with idiopathic pulmonary arterial hypertension and animals with PH and cultured PH-Fibs, respectively. Decreasing NADH pharmacologically with MTOB or genetically blocking CtBP1 with siRNA upregulated the cyclin-dependent genes (p15 and p21) and proapoptotic regulators (NOXA and PERP), attenuated proliferation, corrected the glycolytic reprogramming phenotype of PH-Fibs, and augmented transcription of the anti-inflammatory gene HMOX1. Chromatin immunoprecipitation analysis demonstrated that CtBP1 directly binds the HMOX1 promoter. Treatment of hypoxic mice with MTOB decreased glycolysis and expression of inflammatory genes, attenuated proliferation, and suppressed macrophage numbers and remodeling in the distal pulmonary vasculature. CONCLUSIONS: CtBP1 is a critical factor linking changes in cell metabolism to cell phenotype in hypoxic and other forms of PH and a therapeutic target.

MeSH
adventicie metabolismus patologie MeSH
alkoholoxidoreduktasy genetika metabolismus MeSH
DNA vazebné proteiny genetika metabolismus MeSH
familiární plicní arteriální hypertenze genetika metabolismus patologie MeSH
fenotyp MeSH
fibroblasty metabolismus patologie MeSH
kultivované buňky MeSH
lidé MeSH
myši MeSH
plicní hypertenze metabolismus patologie MeSH
zvířata MeSH
Check Tag
lidé MeSH
myši MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH

Článek

Vasa vasorum in the tunica media and tunica adventitia of the porcine aorta

Annals of anatomy. 2016 ; 205 (-) : 22-36. [pub] 20160201

Ann Anat
ISSN 1618-0402
Medvik
Zdroj

Vasa vasorum supply both the tunica adventitia and the tunica media of major arteries with nutrients and oxygen. We estimated the density of von Willebrand factor-positive profiles of vasa vasorum visible in transversal histological sections of 123 tissue samples collected from five anatomical positions in the porcine aortae of growing pigs (n=25). The animals ranged in age from 0 to 230 days. The tunica media of the thoracic aorta had a greater vasa vasorum density, with microvessels penetrating deeper towards the lumen than in the abdominal aorta. The density of vasa vasorum gradually decreased with age in both the media and the adventitia. The relative depth into which the vasa vasorum penetrated and where they branched remained constant during the ageing and growth of the media. The ratio of the tunica media and tunica adventitia thicknesses did not change in the single aortic segments during ageing. The media of older animals received fewer but equally distributed vasa vasorum. A greater density of vasa vasorum in the media was correlated with greater media thickness and a greater elastin fraction (data on elastin taken from another study on the same samples). Immunohistochemical quantification revealed deeper penetration of vasa vasorum towards the adluminal layers of the tunica media that were hitherto reported to be avascular. The complete primary morphometric data, in the form of continuous variables, have been made available as a supplement. Mapping of the vasa vasorum profile density and position has promising illustrative potential for studies on atherosclerotic and inflammatory neovascularization, aortic aneurysms, and drug distribution from arterial stents in experimental porcine models.

Článek

The contribution of vascular smooth muscle, elastin and collagen on the passive mechanics of porcine carotid arteries

Physiological measurement. 2012 ; 33 (8) : 1335-1351.

Physiol Meas
ISSN 1361-6579
Medvik
Zdroj

The main components responsible for the mechanical behavior of the arterial wall are collagen, elastin, and smooth muscle cells (SMCs) in the medial layer. We determined the structural and mechanical changes in porcine carotid arteries after administration of Triton® X-100, elastase, and collagenase using the inflation-deflation test. The arteries were intraluminarly pressurized from 0 to 200 mmHg, and the outer diameter of the artery was measured. The pressure-strain elastic modulus was determined based on the pressure/diameter ratio. The intima-media thickness, wall thickness, thickness of the tunica adventitia layer, and the area fractions of SMCs, elastin, and collagen within the arterial wall (A(A)(SMC/elastin/collagen, wall)) were measured using stereological methods. The relative changes in the relevant components of the treated samples were as follows: the decrease in A(A)(SMC, wall) after administration of Triton® X-100 was 11% ± 7%, the decrease in A(A)(elastin, wall) after administration of elastase was 40% ± 22%, and the decrease in A(A)(collagen, wall) after the application of collagenase was 51% ± 22%. The Triton® X-100 treatment led to a decrease in the SMC content that was associated with enlargement of the arterial wall (outer diameter) for pressures up to 120 mmHg, and with mechanical stiffening of the arterial wall at higher pressures. Elastase led to a decrease in the elastin content that was associated with enlargement of the arterial wall, but not with stiffening or softening. Collagenase led to a decrease in collagen content that was associated with a change in the stiffness of the arterial wall, although the exact contribution of mechanical loading and the duration of treatment (enlargement) could not be quantified.