Collagen is reduced and disrupted in human aneurysms and dissections of ascending aorta

Borges, Luciano de Figueiredo; Jaldin, Rodrigo Gibin; Dias, Ricardo Ribeiro; Na, Stolf; Michel, Jean‐Baptiste; Gutierrez, Paulo Sampaio

doi:10.1016/j.humpath.2007.08.003

Cited by 90 publications

(87 citation statements)

References 20 publications

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“…[23][24][25] The present study, however, revealed no significant change in either the adventitial or medial collagen content during TAA formation. Although this may suggest a lack of collagen degradation, given previous results establishing a temporal profile of protease production throughout TAA development, 26 it is more likely that collagen degradation and deposition remain balanced in regard to total content.…”

Section: Analysis Of Taa-induced Structural Changescontrasting

confidence: 81%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

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The present study tested the hypothesis that changes in the resident endogenous cellular population accompany alterations in aortic collagen and elastin content during thoracic aortic aneurysm (TAA) development in a murine model. Descending thoracic aortas were analyzed at various time points (2, 4, 8, and 16 weeks) post-TAA induction (0.5 M CaCl 2 , 15 minutes). Aortic tissue sections were subjected to histological staining and morphometric analysis for collagen and elastin, as well as immunostaining for cell-type-specific markers to quantify fibroblasts, myofibroblasts, and smoothmuscle cells. Results were compared with reference control mice processed in the same fashion. Aortic dilatation was accompanied by changes in the elastic architecture that included: a decreased number of elastic lamellae (from 6 to 4); altered area fraction of elastin (elevated at 4 weeks and decreased at 16 weeks); and a decreased area between elastic lamellae (minimum reached at 4 weeks). Total collagen content did not change over time. Increased immunoreactivity for fibroblast and myofibroblast markers was observed at 8-and 16-week post-TAA-induction, whereas immunoreactivity for smooth-muscle cell markers peaked at 4 weeks and returned to baseline by 16 weeks. Therefore, this study demonstrated that changes in aortic elastin content were accompanied by the emergence of a subset of fibroblast-derived myofibroblasts whose altered phenotype may play a significant role in TAA development through the enhancement of extracellular matrix proteolysis.

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Section: Analysis Of Taa-induced Structural Changescontrasting

confidence: 81%

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Jones

Beck

Barbour

et al. 2009

The American Journal of Pathology

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“…In ATA dissections, the microstructure was characterized by a loss of elastin content and a decrease in interlaminar elastin fibres [60]. Furthermore, these fibres were fragmented and irregularly arranged [60], which, as previously mentioned, is also common in ATA dissections with and without accompanying aneurysm [54,56,59], in ATA dissections accompanied by CMD and medionecrosis [59,62], or with severe atherosclerosis [59]. In the control tissue, the structure of elastin was continuous and formed elastin laminae, which were interconnected through interlaminar fibres.…”

Section: Effects Of Diseasementioning

confidence: 69%

“…This trend of decreased number of SMCs in the aortic wall is also common in ageing, hypertension and in presence of atheromatous plaque [88][89][90]94]. Disrupted and irregular elastin lamellae have been observed in the medial layer of dissecting ATAs with and without accompanying aneurysm, with some areas either being devoid of an elastin fibre framework, or having localized elastin fragmentation [56,59]. This was opposed to that seen in the control ATA, where the layers of SMCs were separated by prominent elastin lamellae, which were interconnected by a network of small elastin fibres and collagen fibres.…”

Section: Effects Of Diseasementioning

confidence: 94%

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Tsamis

Krawiec

Vorp

2013

J. R. Soc. Interface.

405

300

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Aortic disease is a significant cause of death in developed countries. The most common forms of aortic disease are aneurysm, dissection, atherosclerotic occlusion and ageing-induced stiffening. The microstructure of the aortic tissue has been studied with great interest, because alteration of the quantity and/or architecture of the connective fibres (elastin and collagen) within the aortic wall, which directly imparts elasticity and strength, can lead to the mechanical and functional changes associated with these conditions. This review article summarizes the state of the art with respect to characterization of connective fibre microstructure in the wall of the human aorta in ageing and disease, with emphasis on the ascending thoracic aorta and abdominal aorta where the most common forms of aortic disease tend to occur.

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“…The alteration of its constituents, collagen and elastin, impair the functional behavior of these tissues inducing ascending aortic diseases such as aneurysms or dissections highly mortal due to the rupture of the vessel [1]. Aortic dissections and ascending aorta aneurysms share the same histopathologic features, situated at the medial layer namely, increase in mucoid substance, fragmentation of elastic fibers, and apparent reduction in the number of smooth muscle cells [2]. A possible mechanism for dissection [3] is that blood pressure-induced stresses exceed the adhesive strength that holds the elastic layers together [4].…”

Section: Introductionmentioning

confidence: 99%

“…In asymptomatic patients with ascending aortic aneurysm, this degradation is not always manifested through the diameter enlargement [6] so an alternative assessment technique is advisable. The conventional histopathological analysis provides the gold standard to evaluate the quality of the aortic wall [2], but its implementation is not straightforward during intervention. Optical techniques such as multiphoton microscopy [3,4] have assessed the degradation of the aortic wall with penetrations of 200μm and, when combined with coherent anti-Stokes Raman spectroscopy is able to distinguish collagen from cholesterol in atherosclerotic arterial tissue [7] quantifying the fiber size, distribution and anisotropy of collagen in healthy arterial wall and in atherosclerotic plaque using image pattern evaluation algorithms.…”

Section: Introductionmentioning

confidence: 99%

Identification of vessel wall degradation in ascending thoracic aortic aneurysms with OCT

Real¹,

Val-Bernal²,

Revuelta³

et al. 2014

Biomed. Opt. Express

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Degradation of the wall of human ascending thoracic aorta has been assessed through Optical Coherence Tomography (OCT). OCT images of the media layer of the aortic wall exhibit micro-structure degradation in case of diseased aortas from aneurysmal vessels. The OCT indicator of degradation depends on the dimension of areas of the media layer where backscattered reflectivity becomes smaller due to a disorder on the morphology of elastin, collagen and smooth muscle cells (SMCs). Efficient pre-processing of the OCT images is required to accurately extract the dimension of degraded areas after an optimized thresholding procedure. OCT results have been validated against conventional histological analysis. The OCT qualitative assessment has achieved a pair sensitivity-specificity of 100%-91.6% in low-high degradation discrimination when a threshold of 4965.88µm 2 is selected. This threshold suggests to have physiological meaning. The OCT quantitative evaluation of degradation achieves a correlation of 0.736 between the OCT indicator and the histological score. This in-vitro study can be transferred to the clinical scenario to provide an intraoperative assessment tool to guide cardiovascular surgeons in open repair interventions.

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Collagen is reduced and disrupted in human aneurysms and dissections of ascending aorta

Cited by 90 publications

References 20 publications

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Alterations in Aortic Cellular Constituents during Thoracic Aortic Aneurysm Development

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Identification of vessel wall degradation in ascending thoracic aortic aneurysms with OCT

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