scholarly journals Differential Protein Expression in Serum of Abdominal Aortic Aneurysm Patients – A Proteomic Approach

2011 ◽  
Vol 42 (5) ◽  
pp. 563-570 ◽  
Author(s):  
B. Pulinx ◽  
F.A.M.V.I. Hellenthal ◽  
K. Hamulyák ◽  
M.P. van Dieijen-Visser ◽  
G.W.H. Schurink ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Protein Expression ◽  
Differential Protein Expression ◽  
Differential Protein ◽  
Proteomic Approach ◽  
Abdominal Aortic

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 9781: Deletion of Prolyl Hydroxylase Domain Protein 2 in Myeloid Lineage suppressed Experimental Abdominal Aortic Aneurysm via NF-κB Inactivation

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Tomotake Tokunou ◽  
Chikahiro Sankoda ◽  
Aya Watanabe ◽  
Yusuke Takahara ◽  
Hiroshi Kojima ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Protein Expression ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Peritoneal Macrophages ◽  
Binding Activity ◽  
Abdominal Aortic ◽  
Domain Protein

Background: Macrophage migration to the vessels is important for vascular inflammation and induces vascular degenerative diseases. Macrophages secrete matrix metalloprotainases (MMPs), which activate many cytokines and digest extracellular matrix of aorta. MMPs play an important role in the progression of aortic aneurysm. We previously reported that non-specific prolyl hydroxylase domain protein (PHD) inhibitor, Cobalt chloride (CoCl2), suppressed MMP-2 and -9 expression and attenuated experimental abdominal aortic aneurysm (AAA) formation in mice. In this report we investigated the myeloid specific PHD2 knockout effect on MMPs expression and aneurysm formation. Methods: Myeloid specific PHD2 conditional knockout (MyPHD2KO) mice were generated. Experimental AAA was induced by periaortic application of Calcium chloride (CaCl2) for 6 weeks. In vitro Lipopolysaccharide (LPS, 100ng/ml) was used to induce MMP-2 and MMP-9 expression with peritoneal macrophages. MMPs mRNA, protein expression and protein activity were analyzed by qRT-PCR, Western blot analysis and Zymography, respectively. ELISA-based NF-κB p65 Transcription Factor Assay was used to examine NF-κB p65 binding activity with consensus DNA binding site. Results: CaCl2-induced AAA was suppressed with MyPHD2KO mice (max diameter of aneurysm: 1.03mm±0.14mm in MyPHD2KO group, 1.63mm±0.34mm in Control AAA group, p<0.01). In peritoneal macrophages CoCl2 reduced LPS-induced MMP-2 and MMP-9 mRNA and protein expression. PHD2 deletion in peritoneal macrophages from MyPHD2KO mice also suppressed LPS-induced MMP-2 and MMP-9 mRNA, protein expression and activity. PHD2 deletion suppressed LPS-induced NF-κB p65 phosphorylation via IκBα stabilization by Western blot analysis. NF-κB p65 binding activity was suppressed in MyPHD2KO macrophages (p<0.01 vs control). Conclusion: Deletion of PHD2 in myeloid lineage attenuated MMPs expression by NF-κB inactivation and suppressed AAA formation. PHD2 in macrophage may be a novel target for cardiovascular disease treatment.

Investigation of Plasma Inflammatory Profile in Diabetic Patients With Abdominal Aortic Aneurysm: A Pilot Study

2018 ◽  
Vol 52 (8) ◽  
pp. 597-601 ◽  
Author(s):  
Fabien Lareyre ◽  
Claudine Moratal ◽  
Julien Chikande ◽  
Elixène Jean-Baptiste ◽  
Réda Hassen-Khodja ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Protein Expression ◽  
Negative Association ◽  
Diabetic Patients ◽  
Protein Biomarkers ◽  
Abdominal Aortic ◽  
Tumor Necrosis Factor Ligand ◽  
Lower Protein ◽  
Inflammatory Profile

Introduction: Clinical studies have unraveled a negative association between diabetes and abdominal aortic aneurysm (AAA), but the mechanisms involved are still poorly understood. The aim of this study was to determine whether diabetic patients with AAA had a distinct plasma inflammatory profile compared to nondiabetic patients. Methods: Plasma samples were obtained from 10 diabetic patients with AAA and 10 nondiabetic patients with AAA. The relative protein expression of 92 inflammatory-related human protein biomarkers was assessed by proximity extension assay technology using Proseek Multiplex Inflammation I kit (Olink). Results: Clinical characteristics were similar in diabetic patients with AAA compared to nondiabetic patients with AAA, the median ages being 67 and 73 years, respectively ( P = .61). The AAA diameters were, respectively, 50 and 49 mm ( P = .72). Among the 92 markers screened, 67 (72.8%) were detected in all samples. Diabetic patients had significantly lower protein expression of C-C motif chemokine 19 (CCL19) and C-C motif chemokine 23 (CCL23; 542.3 vs 980.3, P = .01 and 1236 vs 1406, P = .04, respectively). They tended to have higher expression of tumor necrosis factor ligand superfamily member 14 (TNFSF14) compared to controls (14.6 vs 10.8, P = .05). Conclusion: Diabetic patients with AAA differentially expressed CCL19, CCL23 and TNFSF14 in plasma compared to nondiabetic patients with AAA. Further studies are required to determine whether the markers identified could play a role in the negative association between diabetes and AAA pathogenesis.

scholarly journals A proteomic approach to identify plasma proteins in patients with abdominal aortic aneurysm

2011 ◽  
Vol 7 (10) ◽  
pp. 2855 ◽  
Author(s):  
Tania Gamberi ◽  
Michele Puglia ◽  
Francesca Guidi ◽  
Francesca Magherini ◽  
Luca Bini ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Plasma Proteins ◽  
Proteomic Approach ◽  
Abdominal Aortic

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.

scholarly journals Identification of Potential Plasma Biomarkers for Abdominal Aortic Aneurysm Using Tandem Mass Tag Quantitative Proteomics

Proteomes ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 43 ◽  
Author(s):  
Anders Henriksson ◽  
Markus Lindqvist ◽  
Carina Sihlbom ◽  
Jörgen Bergström ◽  
Dan Bylund
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tandem Mass ◽  
Plasma Biomarkers ◽  
Proteomic Approach ◽  
Abdominal Aortic ◽  
Tandem Mass Tag ◽  
Small Aneurysms ◽  
Mass Tag

Plasma biomarkers that identify abdominal aortic aneurysm (AAA) rupture risk would greatly assist in stratifying patients with small aneurysms. Identification of such biomarkers has hitherto been unsuccessful over a range of studies using different methods. The present study used an alternative proteomic approach to find new, potential plasma AAA biomarker candidates. Pre-fractionated plasma samples from twelve patients with AAA and eight matched controls without aneurysm were analyzed by mass spectrometry applying a tandem mass tag (TMT) technique. Eight proteins were differentially regulated in patients compared to controls, including decreased levels of the enzyme bleomycin hydrolase. The down-regulation of this enzyme was confirmed in an extended validation study using an enzyme-linked immunosorbent assay (ELISA). The TMT-based proteomic approach thus identified novel potential plasma biomarkers for AAA.

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