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Syndromic and non-syndromic aneurysms of the human ascending aorta share activation of the Smad2 pathway
The Journal of pathology, 2009-05, Vol.218 (1), p.131-142
Gomez, Delphine
Al Haj Zen, Ayman
Borges, Luciano F
Philippe, Monique
Gutierrez, Paulo Sampaio
Jondeau, Guillaume
Michel, Jean-Baptiste
Vranckx, Roger
2009
Details
Autor(en) / Beteiligte
Gomez, Delphine
Al Haj Zen, Ayman
Borges, Luciano F
Philippe, Monique
Gutierrez, Paulo Sampaio
Jondeau, Guillaume
Michel, Jean-Baptiste
Vranckx, Roger
Titel
Syndromic and non-syndromic aneurysms of the human ascending aorta share activation of the Smad2 pathway
Ist Teil von
The Journal of pathology, 2009-05, Vol.218 (1), p.131-142
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2009
Link zum Volltext
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Common features such as elastic fibre destruction, mucoid accumulation, and smooth muscle cell apoptosis are co-localized in aneurysms of the ascending aorta of various aetiologies. Recent experimental studies reported an activation of TGF-β in aneurysms related to Marfan (and Loeys-Dietz) syndrome. Here we investigate TGF-β signalling in normal and pathological human ascending aortic wall in syndromic and non-syndromic aneurysmal disease. Aneurysmal ascending aortic specimens, classified according to aetiology: syndromic MFS (n = 15, including two mutations in TGFBR2), associated with BAV (n = 15) or degenerative forms (n = 19), were examined. We show that the amounts of TGF-β1 protein retained within and released by aneurysmal tissue were greater than for control aortic tissue, whatever the aetiology, contrasting with an unchanged TGF-β1 mRNA level. The increase in stored TGF-β1 was associated with enhanced LTBP-1 protein and mRNA levels. These dysregulations of the extracellular ligand are associated with higher phosphorylated Smad2 and Smad2 mRNA levels in the ascending aortic wall from all types of aneurysm. This activation correlated with the degree of elastic fibre fragmentation. Surprisingly, there was no consistent association between the nuclear location of pSmad2 and extracellular TGF-β1 and LTBP-1 staining and between their respective mRNA expressions. In parallel, decorin was focally increased in aneurysmal media, whereas biglycan was globally decreased in aneurysmal aortas. In conclusion, this study highlights independent dysregulations of TGF-β retention and Smad2 signalling in syndromic and non-syndromic aneurysms of the ascending aorta. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.2516
Titel-ID: cdi_proquest_miscellaneous_67121453
Format
–
Schlagworte
Adult
,
Aged
,
Aged, 80 and over
,
Aorta - metabolism
,
Aorta - pathology
,
Aortic Aneurysm - complications
,
Aortic Aneurysm - genetics
,
Aortic Aneurysm - metabolism
,
bicuspid aortic valves
,
Biological and medical sciences
,
Biomarkers - analysis
,
Blood and lymphatic vessels
,
Cardiology. Vascular system
,
Case-Control Studies
,
Cell Differentiation
,
decorin
,
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
,
Gene Expression
,
Humans
,
Immunoblotting - methods
,
Immunohistochemistry
,
Investigative techniques, diagnostic techniques (general aspects)
,
Latent TGF-beta Binding Proteins - analysis
,
Latent TGF-beta Binding Proteins - genetics
,
LTBP-1
,
Marfan syndrome
,
Marfan Syndrome - complications
,
Marfan Syndrome - genetics
,
Marfan Syndrome - metabolism
,
Medical sciences
,
Middle Aged
,
Muscle, Smooth, Vascular - pathology
,
PAI-1
,
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
,
proteoglycans
,
Reverse Transcriptase Polymerase Chain Reaction
,
RNA, Messenger - analysis
,
Signal Transduction - physiology
,
Smad2 Protein - analysis
,
Smad2 Protein - genetics
,
Smad2 Protein - metabolism
,
Statistics, Nonparametric
,
TGF-β
,
Transforming Growth Factor beta1 - analysis
,
Transforming Growth Factor beta1 - genetics
,
Transforming Growth Factor beta1 - metabolism
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