scholarly journals Galectin-3 as a Biomarker for Stratifying Abdominal Aortic Aneurysm Size in a Taiwanese Population

2021 ◽  
Vol 8 ◽  
Author(s):  
Hsin-Ying Lu ◽  
Chun-Ming Shih ◽  
Shih-Hsien Sung ◽  
Alexander T. H. Wu ◽  
Tsai-Mu Cheng ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Characteristic Curve ◽  
Multivariate Logistic Regression Analysis ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Abdominal Aortic ◽  
Galectin 3 ◽  
Inflammatory Processes ◽  
And Control

Abdominal aortic aneurysm (AAA) ruptures are unpredictable and lethal. A biomarker predicting AAA rupture risk could help identify patients with small, screen-detected AAAs. Galectin-3 (Gal-3), a β-galactosidase–binding lectin, is involved in inflammatory processes and may be associated with AAA incidence. We investigated whether Gal-3 can be used as a biomarker of AAA size. Plasma Gal-3 protein concentrations were examined in patients with AAA (n = 151) and control patients (n = 195) using Human ProcartaPlex multiplex and simplex kits. Circulating Gal-3 levels were significantly higher in patients with AAA than in control patients. The area under the receiver operating characteristic curve for Gal-3 was 0.91. Multivariate logistic regression analysis revealed a significant association between Gal-3 level and the presence of AAA. Circulating Gal-3 levels were significantly correlated with aortic diameter in a concentration-dependent manner. In conclusion, higher plasma Gal-3 concentrations may be a useful biomarker of AAA progression.

Increased galectin-3 levels are associated with abdominal aortic aneurysm progression and inhibition of galectin-3 decreases elastase-induced AAA development

2017 ◽  
Vol 131 (22) ◽  
pp. 2707-2719 ◽  
Author(s):  
Carlos-Ernesto Fernandez-García ◽  
Carlos Tarin ◽  
Raquel Roldan-Montero ◽  
Diego Martinez-Lopez ◽  
Monica Torres-Fonseca ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Protein Expression ◽  
Potential Role ◽  
Control Group ◽  
Mrna Levels ◽  
Abdominal Aortic ◽  
Stat3 Phosphorylation ◽  
Galectin 3 ◽  
Mrna And Protein Expression

Abdominal aortic aneurysm (AAA) evolution is unpredictable and no specific treatment exists for AAA, except surgery to prevent aortic rupture. Galectin-3 has been previously associated with CVD, but its potential role in AAA has not been addressed. Galectin-3 levels were increased in the plasma of AAA patients (n=225) compared with the control group (n=100). In addition, galectin-3 concentrations were associated with the need for surgical repair, independently of potential confounding factors. Galectin-3 mRNA and protein expression were increased in human AAA samples compared with healthy aortas. Experimental AAA in mice was induced via aortic elastase perfusion. Mice were treated intravenously with the galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every other day) or saline. Similar to humans, galectin-3 serum and aortic mRNA levels were also increased in elastase-induced AAA mice compared with control mice. Mice treated with MCP showed decreased aortic dilation, as well as elastin degradation, vascular smooth muscle cell (VSMC) loss, and macrophage content at day 14 postelastase perfusion compared with control mice. The underlying mechanism(s) of the protective effect of MCP was associated with a decrease in galectin-3 and cytokine (mainly CCL5) mRNA and protein expression. Interestingly, galectin-3 induced CCL5 expression by a mechanism involving STAT3 activation in VSMC. Accordingly, MCP treatment decreased STAT3 phosphorylation in elastase-induced AAA. In conclusion, increased galectin-3 levels are associated with AAA progression, while galectin-3 inhibition decreased experimental AAA development. Our data suggest the potential role of galectin-3 as a therapeutic target in AAA.

Abstract 503: Chronic Kidney Disease is a Risk for Abdominal Aortic Aneurysm but Diabetes Mellitus is a Protective Factor in Japanese

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Hidemi Takeuchi ◽  
Haruhito Uchida ◽  
Michihiro Okuyama ◽  
Ryoko Umebayashi ◽  
Yuki Kakio ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Abdominal Aortic Aneurysm ◽  
Kidney Disease ◽  
Aortic Aneurysm ◽  
Protective Factor ◽  
Multivariate Logistic Regression Analysis ◽  
Asian Population ◽  
Abdominal Aortic

Objective: Abdominal aortic aneurysm (AAA) is the most common aortic aneurysm. Chronic kidney disease (CKD) and diabetes mellitus (DM) are considered as risk factors for cardiovascular diseases. However, the association between CKD and AAA remains unknown. Although DM has been reported to exert protective effect on the incidence and development of AAA in western population, such protective role of DM was not explored in the Asian population. The purpose of this study was to determine the relationship of CKD and DM and the presence of AAA. We performed a cross-sectional retrospective case-control study in Asian population. Methods and Results: We enrolled 261 patients with AAA (AAA+) and age-and-sex matched 261 patients without AAA (AAA-) at two hospitals between 2008 and 2014, and examined the association between the risk factors and the presence of AAA. Furthermore, to investigate AAA prevalencein each group, we enrolled 1126 patients with CKD and 400 patients with DM. The presence of CKD in patients with AAA+ was significantly higher than that in patients with AAA- (AAA+; 65 %, AAA-; 52 %, P = 0.004). The presence of DM in patients with AAA+ was significantly lower than that in patients with AAA- (AAA+; 17 %, AAA-; 35 %, P < 0.001). A multivariate logistic regression analysis demonstrated that hypertension, ischemic heart disease and CKD were independent determinants, whereas, DM was the only independent protective factor, for the presence of AAA. The prevalence of AAA in patients with CKD 65 years old and above was 5.1 %, whereas, that in patients with DM 65 years old and above was only 0.6 %. Conclusion: CKD is a positively associated with the presence of AAA. In contrast, DM is a negatively associated with the presence of AAA.

scholarly journals Association of Neutrophil–Lymphocyte and Platelet–Lymphocyte Ratio with Adverse Events in Endovascular Repair for Abdominal Aortic Aneurysm

2021 ◽  
Vol 10 (5) ◽  
pp. 1083
Author(s):  
Maria P. Ntalouka ◽  
Petroula Nana ◽  
George N. Kouvelos ◽  
Konstantinos Stamoulis ◽  
Konstantinos Spanos ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Adverse Events ◽  
Characteristic Curve ◽  
Endovascular Aneurysm Repair ◽  
Adverse Cardiovascular Event ◽  
Neutrophil Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Platelet Lymphocyte Ratio ◽  
Abdominal Aortic

The association of chronic inflammatory markers with the clinical outcome after endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA) was investigated. We included 230 patients, treated electively with EVAR. The values of neutrophil–lymphocyte ratio (NLR) and platelet–lymphocyte ratio (PLR) were measured pre- and postoperatively. Any major adverse cardiovascular event (MACE) and acute kidney injury (AKI) were recorded. Adverse events occurred in 12 patients (5.2%). Seven patients suffered from MACE and five from AKI. Median NLR and PLR values were significantly increased after the procedure (NLR: from 3.34 to 8.64, p < 0.001 and PLR: from 11.37 to 17.21, p < 0.001). None of the patients or procedure characteristics were associated with the occurrence of either a MACE or AKI. Receiver operating characteristic curve analysis showed that postoperative NLR and PLR were strongly associated with AKI. A threshold postoperative NLR value of 9.9 was associated with the occurrence of AKI, with a sensitivity of 80% and specificity of 81%. A threshold postoperative PLR value of 22.8 was associated with the occurrence of AKI, with a sensitivity of 80% and specificity of 83%. Postoperative NLR and PLR have been associated with the occurrence of AKI after EVAR for AAA.

scholarly journals Role of MicroRNA-103a Targeting ADAM10 in Abdominal Aortic Aneurysm

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Tong Jiao ◽  
Ye Yao ◽  
Bo Zhang ◽  
Da-Cheng Hao ◽  
Qing-Feng Sun ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Protein Expression ◽  
Mrna Expression ◽  
Posttranscriptional Regulation ◽  
Specific Inhibitor ◽  
Cellular Level ◽  
Vital Role ◽  
Abdominal Aortic ◽  
And Control

MicroRNAs (miRNAs) are deregulated in various vascular ailments including abdominal aortic aneurysm (AAA). MiR-103 is involved in vascular, metabolic, and malignant diseases, but whether it participates in the pathogenesis of AAA remains elusive. ADAM10 plays a vital role in the formation of aneurysm, but whether miRs modulate its activity during AAA formation is totally unknown. In this study, we detected the significantly increased protein expression of ADAM10 in angiotensin II induced murine AAA specimens, while the mRNA expression of ADAM10 was similar between AAA and control, suggesting the posttranscriptional regulation. The ADAM10 specific inhibitor GI254023X dramatically reduced the macrophage infiltration of murine abdominal aorta. Bioinformatic predictions suggest that ADAM10 is the target of miR-103a/107 but the binding site is exclusive. At the cellular level, miR-103a-1 suppressed the protein expression of ADAM10, while antisense miR-103a-1 increased its expression. Particularly, with the progression of murine AAA, the mRNA expression of miR-103a/107 substantially decreased and the protein expression of ADAM10 greatly increased. Together, our data afford the new insight that miR-103a inhibited AAA growth via targeting ADAM10, which might be a promising therapeutic strategy to alleviate AAA.

A Pilot Study of Protein Microarray for Simultaneous Analysis of 274 Cytokines Between Abdominal Aortic Aneurysm and Normal Aorta

Angiology ◽  
2019 ◽  
Vol 70 (9) ◽  
pp. 830-837 ◽  
Author(s):  
Li Yuwen ◽  
Yang Ciqiu ◽  
Shi Yi ◽  
Liu Ruilei ◽  
Lai Yuanhui ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Expression Profile ◽  
Protein Microarray ◽  
Cytokine Expression ◽  
Protein Array ◽  
Differentially Expressed ◽  
Cytokine Expression Profile ◽  
Abdominal Aortic ◽  
And Control

Cytokines play an important role in the pathogenesis of abdominal aortic aneurysm (AAA). We evaluated the cytokine expression profile of large AAA walls using a 274-cytokine protein array. We hypothesized that AAAs are characterized by an inflammatory, chemotactic cytokine profile. We investigated the cytokine expression profile of 12 patients with AAA and 6 nonaneurysmal controls using an antibody-based protein array. The array generated antibodies against homogenized human aortic tissues to validate the cytokines differentially expressed in AAAs and normal aortas. Data were quantified using fluorescent signal intensities and statistically analyzed by the t test. Fifty-nine cytokines were differentially expressed between the AAA and control samples. Of the 35 selected cytokines that had relative expression >1000, 29 were significantly higher and 6 were lower in AAA samples than in controls. They respectively belonged to CC chemokines, CXC chemokines, pro-inflammatory cytokines, growth factors, proteolytic proteins and inhibitors, and cell adhesion cytokines. Our results show that distinct cytokines are involved in AAAs and suggest that the pathways involving these cytokines may be associated with the pathogenesis and development of AAAs. These findings, if confirmed by larger studies, may suggest treatment targets.

scholarly journals Dissecting Abdominal Aortic Aneurysm Is Aggravated by Genetic Inactivation of LIGHT (TNFSF14)

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1518
Author(s):  
Andrea Herrero-Cervera ◽  
Carla Espinós-Estévez ◽  
Susana Martín-Vañó ◽  
Alida Taberner-Cortés ◽  
María Aguilar-Ballester ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Maximum Diameter ◽  
Dependent Manner ◽  
Genetic Inactivation ◽  
Abdominal Aortic ◽  
The Impact ◽  
Role Of Light

Abdominal aortic aneurysm (AAA), is a complex disorder characterized by vascular vessel wall remodeling. LIGHT (TNFSF14) is a proinflammatory cytokine associated with vascular disease. In the present study, the impact of genetic inactivation of Light was investigated in dissecting AAA induced by angiotensin II (AngII) in the Apolipoprotein E-deficient (Apoe−/−) mice. Studies in aortic human (ah) vascular smooth muscle cells (VSMC) to study potential translation to human pathology were also performed. AngII-treated Apoe−/−Light−/− mice displayed increased abdominal aorta maximum diameter and AAA severity compared with Apoe−/− mice. Notably, reduced smooth muscle α-actin+ area and Acta2 and Col1a1 gene expression were observed in AAA from Apoe−/−Light−/− mice, suggesting a loss of VSMC contractile phenotype compared with controls. Decreased Opn and augmented Sox9 expression, which are associated with detrimental and non-contractile osteochondrogenic VSMC phenotypes, were also seen in AngII-treated Apoe−/−Light−/− mouse AAA. Consistent with a role of LIGHT preserving VSMC contractile characteristics, LIGHT-treatment of ahVSMCs diminished the expression of SOX9 and of the pluripotency marker CKIT. These effects were partly mediated through lymphotoxin β receptor (LTβR) as the silencing of its gene ablated LIGHT effects on ahVSMCs. These studies suggest a protective role of LIGHT through mechanisms that prevent VSMC trans-differentiation in an LTβR-dependent manner.

scholarly journals Efficient Suppression of Abdominal Aortic Aneurysm Expansion in Rats through Systemic Administration of Statin-Loaded Nanomedicine

2020 ◽  
Vol 21 (22) ◽  
pp. 8702
Author(s):  
Natsumi Fukuhara ◽  
Yuto Honda ◽  
Nao Ukita ◽  
Makoto Matsui ◽  
Yutaka Miura ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Polymeric Micelles ◽  
Polymeric Micelle ◽  
Dependent Manner ◽  
Cancer Treatments ◽  
Abdominal Aortic ◽  
Efficient Suppression ◽  
Life Threatening ◽  
Dose Dependent

Abdominal aortic aneurysm (AAA) is a life-threatening disease. However, no systemically injectable drug has been approved for AAA treatment due to low bioavailability. Polymeric micelles are nanomedicines that have the potential to improve therapeutic efficacy by selectively delivering drugs into disease sites, and research has mainly focused on cancer treatments. Here, we developed a statin-loaded polymeric micelle to treat AAAs in rat models. The micelle showed medicinal efficacy by preventing aortic aneurysm expansion in a dose-dependent manner. Furthermore, the micelle-injected group showed decreased macrophage infiltration and decreased matrix metalloproteinase-9 activity in cases of AAA.

scholarly journals Galectin-3 Modulates Macrophage Activation and Contributes Smooth Muscle Cells Apoptosis in Abdominal Aortic Aneurysm Pathogenesis

2020 ◽  
Vol 21 (21) ◽  
pp. 8257
Author(s):  
Hsin-Ying Lu ◽  
Chun-Ming Shih ◽  
Chun-Yang Huang ◽  
Alexander T. H. Wu ◽  
Tsai-Mu Cheng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Messenger Rna ◽  
Macrophage Activation ◽  
In Vitro Study ◽  
Abdominal Aortic ◽  
Galectin 3 ◽  
Apoe Knockout Mice

Galectin-3 (Gal-3) is a 26-kDa lectin that regulates many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to abdominal aortic aneurysm (AAA) progression by enhancing monocyte chemoattraction through macrophage activation. We analyzed the plasma levels of Gal-3 in 76 patients with AAA (AAA group) and 97 controls (CTL group) as well as in angiotensin II (Ang-II)-infused ApoE knockout mice. Additionally, conditioned media (CM) were used to polarize THP-1 monocyte to M1 macrophages with or without Gal-3 inhibition through small interfering RNA targeted deletion to investigate whether Gal-3 inhibition could attenuate macrophage-induced inflammation and smooth muscle cell (SMC) apoptosis. Our results showed a markedly increased expression of Gal-3 in the plasma and aorta in the AAA patients and experimental mice compared with the CTL group. An in vitro study demonstrated that the M1 cells exhibited increased Gal-3 expression. Gal-3 inhibition markedly decreased the quantity of macrophage-induced inflammatory regulators, including IL-8, TNF-α, and IL-1β, as well as messenger RNA expression and MMP-9 activity. Moreover, Gal-3-deficient CM weakened SMC apoptosis through Fas activation. These findings prove that Gal-3 may contribute to AAA progression by the activation of inflammatory macrophages, thereby promoting SMC apoptosis.

Abstract 668: The Role of IL-27 Receptor Signaling in the Development of Abdominal Aortic Aneurysm

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Iuliia Peshkova ◽  
Petr Makhov ◽  
Vivianly Hou ◽  
Ekaterina Koltsova
Keyword(s):  
T Cells ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Inflammatory Cytokines ◽  
Aortic Wall ◽  
Lymphoid Cells ◽  
Dependent Manner ◽  
Enhanced Production ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) is a cardiovascular disease, which is characterized by aortic wall dilation with subsequent rupture and internal bleeding. Inflammatory reactions in the vessel wall are likely essential for AAA pathogenesis, just like they are important for the development of another vascular pathology- atherosclerosis, which can predispose to AAA formation in a context-dependent manner. While inflammatory cytokines were shown to promote atherosclerosis and AAA, little is known about contribution of anti-inflammatory cytokines with regard to their ability to control vascular inflammation. Interleukin (IL)-27 signaling is required to suppress atherosclerosis development but its function in AAA remains unknown. We utilize Angiotensin II (AngII) model to evaluate the role of IL-27R signaling in pathogenesis of AAA. AngII containing pumps were surgically implanted into Il27ra-/- x Ldlr-/-; Il27ra -/- x Apoe-/- and Il27ra+/- littermate controls and AAA progression was analyzed 4 weeks later. Surprisingly, we found attenuated AAA progression in Il27ra-/- mice compared to Il27ra+/- and wt counterparts. The latter developed large AAA with visual hemorrhage into the artery wall, while Il27ra-/- mice developed small AAA with fewer myeloid cells and T cells. Moreover, opposite to aortic arches, T cells in abdominal aortas of Il27ra-/- mice produced less inflammatory IL-17A, while IFNγ production was unchanged. Interestingly, we found enhanced production of “Th2-like” cytokines IL-4 and IL-13, by NK cells and Type 2 Innate lymphoid cells (ILC2) in Il27ra deficient mice, which correlated with the protection from AAA. Overall, we conclude that immunoregulatory cytokine IL-27 can differentially control atherosclerosis and AAA development by regulating innate and adaptive immune cell recruitment and cytokine production in the aortic wall.

Sign in / Sign up

Export Citation Format

Share Document