VOJNOSANIT PREGL

2010

DOI: 10.2298/vsp1012959t

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Histochemical and immunohistochemical analysis of ruptured atherosclerotic abdominal aortic aneurysm wall

Irena Tanasković¹,

Aleksandra Mladenovic-Mihailovic²,

Slavica Usaj-Knezevic³

et al.

Abstract: Rupture of aneurysm occurs from the primary intimal disruption, which spreads into thinned out media and adventitia. Rupture is caused by unstable atherom, hypocellularity, loss of contractile characteristics of smooth muscle cells in intima and media, neovascularization of the media, as well as by the activity of the macrophages in the lesion.

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Mast Cell Protease Functions Related To Aaa1

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Cited by 8 publications

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“…2b) has been shown before [17,41,42]. We found most actin- and vimentin-positive elements in medium-sized AAAs (fig.…”

Section: Discussionsupporting

confidence: 84%

Asymptomatic Abdominal Aortic Aneurysms Show Histological Signs of Progression: A Quantitative Histochemical Analysis

³

et al. 2012

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Objective: Abdominal aortic aneurysm (AAA) is a serious disease due to its covert nature, relatively high prevalence and fatal prognosis in the case of rupture. To obtain new insights into AAA pathogenesis, we examined the relationships between histopathology, multiplex in vitro immunoassay data, diameter and symptomatology. Methods: In a prospective, non-randomised study, we evaluated samples from 6 normal infrarenal aortae and 65 AAA patients (65 walls, 55 thrombi). The AAA patients were either asymptomatic (n = 44), symptomatic (n = 7) or with ruptured AAA (n = 14). The AAA diameter was classified as small (<5 cm, n = 18), medium (5–7 cm, n = 26) and large (>7 cm, n = 21). We quantified the histopathology of the AAA wall and the adjacent thrombus. We assessed the expression of proteins in the same samples. Results: Asymptomatic AAAs had walls with more abundant inflammatory infiltrates, lower amounts of PAI-1, a higher number of tPA-positive elements, a tendency towards decreased collagen content, whereas the adjacent thrombi had a greater concentration of VCAM-1 and MMP-2 when compared with symptomatic AAAs. Compared with the aneurysmatic aorta, the normal aorta contained less collagen and more elastin, actin, desmin and PAI-1-positive elements; in addition, it was more vascular. Medium-sized AAAs were the most actin and vimentin rich, and large AAAs were the most vascular. Conclusion: Our results show that asymptomatic AAA walls often have more potentially deleterious histopathological alterations than symptomatic AAA walls. This result indicates that a progression from an asymptomatic AAA to rupture can be expected and screening patients who are at risk of rupture could be beneficial.

“…2b) has been shown before [17,41,42]. We found most actin- and vimentin-positive elements in medium-sized AAAs (fig.…”

Section: Discussionsupporting

confidence: 84%

Asymptomatic Abdominal Aortic Aneurysms Show Histological Signs of Progression: A Quantitative Histochemical Analysis

³

et al. 2012

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Objective: Abdominal aortic aneurysm (AAA) is a serious disease due to its covert nature, relatively high prevalence and fatal prognosis in the case of rupture. To obtain new insights into AAA pathogenesis, we examined the relationships between histopathology, multiplex in vitro immunoassay data, diameter and symptomatology. Methods: In a prospective, non-randomised study, we evaluated samples from 6 normal infrarenal aortae and 65 AAA patients (65 walls, 55 thrombi). The AAA patients were either asymptomatic (n = 44), symptomatic (n = 7) or with ruptured AAA (n = 14). The AAA diameter was classified as small (<5 cm, n = 18), medium (5–7 cm, n = 26) and large (>7 cm, n = 21). We quantified the histopathology of the AAA wall and the adjacent thrombus. We assessed the expression of proteins in the same samples. Results: Asymptomatic AAAs had walls with more abundant inflammatory infiltrates, lower amounts of PAI-1, a higher number of tPA-positive elements, a tendency towards decreased collagen content, whereas the adjacent thrombi had a greater concentration of VCAM-1 and MMP-2 when compared with symptomatic AAAs. Compared with the aneurysmatic aorta, the normal aorta contained less collagen and more elastin, actin, desmin and PAI-1-positive elements; in addition, it was more vascular. Medium-sized AAAs were the most actin and vimentin rich, and large AAAs were the most vascular. Conclusion: Our results show that asymptomatic AAA walls often have more potentially deleterious histopathological alterations than symptomatic AAA walls. This result indicates that a progression from an asymptomatic AAA to rupture can be expected and screening patients who are at risk of rupture could be beneficial.

“…A higher degree of immune cell infiltration and inflammatory response was observed in ruptured AAA than in stable AAA [45]. Histochemical and immunohistochemical analyses have shown that rupture of AAA occurs because of unstable atherom, hypocellularity, and loss of contractile characteristics of smooth muscle cells in the intima and media [46]. The structure and strength of the aortic wall, mechanical characteristics of the aorta, and cellular and proteolytic components of the AAA wall can directly contribute to AAA rupture [47].…”

Section: Discussionmentioning

confidence: 99%

Identification of abdominal aortic aneurysm subtypes based on mechanosensitive genes

Sheng,

Zeng,

Huang

et al. 2024

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Background Rupture of abdominal aortic aneurysm (rAAA) is a fatal event in the elderly. Elevated blood pressure and weakening of vessel wall strength are major risk factors for this devastating event. This present study examined whether the expression profile of mechanosensitive genes correlates with the phenotype and outcome, thus, serving as a biomarker for AAA development. Methods In this study, we identified mechanosensitive genes involved in AAA development using general bioinformatics methods and machine learning with six human datasets publicly available from the GEO database. Differentially expressed mechanosensitive genes (DEMGs) in AAAs were identified by differential expression analysis. Molecular biological functions of genes were explored using functional clustering, Protein–protein interaction (PPI), and weighted gene co-expression network analysis (WGCNA). According to the datasets (GSE98278, GSE205071 and GSE165470), the changes of diameter and aortic wall strength of AAA induced by DEMGs were verified by consensus clustering analysis, machine learning models, and statistical analysis. In addition, a model for identifying AAA subtypes was built using machine learning methods. Results 38 DEMGs clustered in pathways regulating ‘Smooth muscle cell biology’ and ‘Cell or Tissue connectivity’. By analyzing the GSE205071 and GSE165470 datasets, DEMGs were found to respond to differences in aneurysm diameter and vessel wall strength. Thus, in the merged datasets, we formally created subgroups of AAAs and found differences in immune characteristics between the subgroups. Finally, a model that accurately predicts the AAA subtype that is more likely to rupture was successfully developed. Conclusion We identified 38 DEMGs that may be involved in AAA. This gene cluster is involved in regulating the maximum vessel diameter, degree of immunoinflammatory infiltration, and strength of the local vessel wall in AAA. The prognostic model we developed can accurately identify the AAA subtypes that tend to rupture.

“…They found that significant α-SMA expressions in the media of the occlusive aorta and aneurysmal neck, but SMCs in the aneurysmal dilated region were disrupted and disorganized. Tanaskovic et al ( 5 ) found by an immunohistochemical study that α-SMA and vimentin were positively stained in SMCs of the media and in the margins of the plaques. Hou et al ( 6 ) used western blotting and immunohistochemical studies to investigate α-SMA expression in the dissected thoracic aorta and found that α-SMA expressions were significantly downregulated in medial SMCs compared with those in a normal aorta ( 6 ).…”

Section: Discussionmentioning

confidence: 99%

Aortic ⍺-smooth muscle actin expressions in aortic disorders and coronary artery disease: An immunohistochemical study

¹

,

Wu²

2018

Anatol J Cardiol

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Objective:The is to report immunohistochemical observations of aortic α-smooth muscle actin (SMA) expressions in patients with aortic aneurysm, acute aortic dissection, and coronary artery disease and to discuss phenotypic switching of smooth muscle cells (SMCs) of these lesions.Methods:Forty-nine consecutive patients scheduled for surgical treatment for acute type A aortic dissection (20 patients), aortic aneurysm (9 patients), and coronary artery disease (20 patients) were included. Surgical specimens of the aorta were obtained and prepared for hematoxylin and eosin and immunohistochemical stainings.Results:A comparison of aortic structural changes between the three groups showed that patients with coronary artery disease had the least severe aorta degeneration with the most intense α-SMA positivity. Aortic structural impairment was the most severe in patients with aortic dissection, whereas α-SMA positivity was more intense in patients with aortic dissection than in those with aortic aneurysm.Conclusion:Disparities in α-SMA expressions in the aortic tissues of the three groups represent the extent of SMC degenerations or a phenotypic switching between contractile and synthetic SMCs. The results imply severe SMC degenerations in patients with aortic aneurysm, which may be beneficial because of the production of extracellular matrix necessary for healing of the vascular wall, but severe disruptions in elastic fibers in patients with aortic dissection. Patients with coronary artery disease show slight SMC degeneration and phenotypic switching among the three groups. The possible apoptotic and genetic mechanisms of aortic structural impairments warrant further elaborations.

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