scholarly journals Screening key genes for abdominal aortic aneurysm based on gene expression omnibus dataset

2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Li Wan ◽  
Jingyong Huang ◽  
Haizhen Ni ◽  
Guanfeng Yu
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Gene Expression Omnibus ◽  
Abdominal Aortic ◽  
Key Genes

scholarly journals Identification of key genes associated with the human abdominal aortic aneurysm based on the gene expression profile

2015 ◽  
Vol 12 (6) ◽  
pp. 7891-7898 ◽  
Author(s):  
XUDONG CHEN ◽  
CHENGFEI ZHENG ◽  
YUNJUN HE ◽  
LU TIAN ◽  
JIANHUI LI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Abdominal Aortic ◽  
Key Genes

P3114Protective effect of SOCS1-based therapy in experimental abdominal aortic aneurysm

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Bernal Uribe ◽  
L Lopez-Sanz ◽  
A Melgar ◽  
S La-Manna ◽  
L Jimenez-Castilla ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Janus Kinase ◽  
Toxic Dose ◽  
Altered Expression ◽  
Abdominal Aortic ◽  
Stat Pathway

Abstract Introduction Abdominal aortic aneurysm (AAA) is a multifactorial vascular disease characterized by chronic inflammation, oxidative stress and proteolytic activity in the aortic wall, which contribute to extracellular matrix degradation and aortic dilation. Altered expression and activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway have been implicated in several cardiovascular diseases including atherosclerosis and aneurysm formation. Suppressors of cytokine signaling (SOCS) are key negative regulators of JAK/STAT pathway and have been considered an attractive target for therapeutic intervention. AIM We hypothesize that SOCS1 protein could influence AAA development by inhibiting JAK activity and, consequently, STAT activation and target gene expression. Therefore, this study investigates the effect of a SOCS1-derived synthetic peptide in a rodent model of AAA and in cultured vascular smooth muscle cells (VSMC). Methods Experimental AAA was induced in C57BL/6 mice (males, 12 weeks old) by transient elastase perfusion of the aorta. Mice were randomly divided into control (vehicle, i.p.) and treatment (SOCS1 peptide, 3 mg/kg/day, i.p.) groups. Fourteen days after AAA induction, mice were sacrificed, and aorta segments were collected for histology (n=10/group) and mRNA and protein expression analysis (n=8/group). Results Compared to the AAA control group, SOCS1-treated mice exhibited a significant decrease in aortic diameter (68±6% vs. control; p<0.005) and aortic wall thickness, (67±3% vs. control; p<0.001). Histological analyses of aortic tissues showed a higher content of VSMC (α-actin) along with reduced leukocyte infiltration (macrophages, neutrophils and T-cells) and oxidative stress markers (superoxide anion and 8-hydroxyguanosine) in SOCS1-treated mice. SOCS1 therapy also attenuated the gene expression of inflammatory cytokines (CCL2, CCL5, TNF, IFNγ) and matrix metalloproteinases (MMP2, MMP9) in aortic lesions, and altered the expression levels of macrophage M1 (ArgII, iNOS) and M2 (ArgI, CD206) polarization markers. In vitro experiments in murine VSMC revealed that SOCS1 peptide prevented the expression of cytokines and chemokines induced by non-toxic dose of elastase (5 ug/ml, 24 hours). Effects of SOCS1 treatment were accompanied by a reduction in STAT1 and STAT3 phosphorylation and gene expression, both in AAA lesions and cultured VSMC. Conclusion Our results suggest that SOCS1 peptide presents protective effects in experimental AAA by suppressing JAK/STAT pathway-mediated inflammation. Acknowledgement/Funding MINECO-FEDER (SAF2015-63696-R), ISCII (FIS-FEDER PI17/01495), Spanish Society of Arteriosclerosis.

scholarly journals Transcriptional profiling and network analysis of the murine angiotensin II-induced abdominal aortic aneurysm

2011 ◽  
Vol 43 (17) ◽  
pp. 993-1003 ◽  
Author(s):  
Joshua M. Spin ◽  
Mark Hsu ◽  
Junya Azuma ◽  
Maureen M. Tedesco ◽  
Alicia Deng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Network Analysis ◽  
Aortic Aneurysm ◽  
Mapk Signaling ◽  
Aortic Dilatation ◽  
Ang Ii ◽  
Abdominal Aortic ◽  
Aneurysm Development

We sought to characterize temporal gene expression changes in the murine angiotensin II (ANG II)-ApoE−/− model of abdominal aortic aneurysm (AAA). Aortic ultrasound measurements were obtained over the 28-day time-course. Harvested suprarenal aortic segments were evaluated with whole genome expression profiling at 7, 14, and 28 days using the Agilent Whole Mouse Genome microarray platform and Statistical Analysis of Microarrays at a false discovery rate of <1%. A group of angiotensin-treated mice experienced contained rupture (CR) within 7 days and were analyzed separately. Progressive aortic dilatation occurred throughout the treatment period. However, the numerous early expression differences between ANG II-treated and control were not sustained over time. Ontologic analysis revealed widespread upregulation of inflammatory, immune, and matrix remodeling genes with ANG II treatment, among other pathways such as apoptosis, cell cycling, angiogenesis, and p53 signaling. CR aneurysms displayed significant decreases in TGF-β/BMP-pathway signaling, MAPK signaling, and ErbB signaling genes vs. non-CR/ANG II-treated samples. We also performed literature-based network analysis, extracting numerous highly interconnected genes associated with aneurysm development such as Spp1, Myd88, Adam17 and Lox. 1) ANG II treatment induces extensive early differential expression changes involving abundant signaling pathways in the suprarenal abdominal aorta, particularly wide-ranging increases in inflammatory genes with aneurysm development. 2) These gene expression changes appear to dissipate with time despite continued growth, suggesting that early changes in gene expression influence disease progression in this AAA model, and that the aortic tissue adapts to prolonged ANG II infusion. 3) Network analysis identified nexus genes that may constitute aneurysm biomarkers or therapeutic targets.

scholarly journals Biomechanics and gene expression in abdominal aortic aneurysm

2014 ◽  
Vol 60 (6) ◽  
pp. 1640-1647.e2 ◽  
Author(s):  
Christian Reeps ◽  
Sebastian Kehl ◽  
Fadwa Tanios ◽  
Jonas Biehler ◽  
Jaroslav Pelisek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Abdominal Aortic

scholarly journals Microarray-based Gene Expression Profiling of Abdominal Aortic Aneurysm

2016 ◽  
Vol 52 (1) ◽  
pp. 47-55 ◽  
Author(s):  
H.Z. Butt ◽  
N. Sylvius ◽  
M.K. Salem ◽  
J.B. Wild ◽  
N. Dattani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Abdominal Aortic

scholarly journals Gene Expression in Patients With Abdominal Aortic Aneurysm – More Than Immunological Mechanisms Involved

2019 ◽  
pp. 385-394 ◽  
Author(s):  
M PRUCHA ◽  
P SEDIVY ◽  
P STADLER ◽  
P ZDRAHAL ◽  
V MATOSKA ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Intracellular Signaling ◽  
Expression Profiles ◽  
Gene List ◽  
Cytokine Signaling ◽  
Abdominal Aortic ◽  
Immunological Mechanisms ◽  
Two Samples

Abdominal aortic aneurysm (AAA) is a serious condition of unclear pathogenesis and progression. Two samples were collected from 48 patients during AAA surgery. One sample was collected from the aneurysm, the other from the aneurysm proximal neck where the tissue did not exhibit any aneurysmal changes. Subsequently, gene expression profiles using microarrays (Illumina) were compared in RNA extracted from the samples. Overall, 2,185 genes were found to be upregulated and 2,100 downregulated; from which 158 genes had a different expression with FDR<0.05 (False Discovery Rate) and FC≥2 (Fold Change). Of this number, 115 genes were over-expressed and 43 under-expressed. The analysis of the gene list based on their biological pathways revealed that the regulation of inflammation was mediated by chemokine and cytokine signaling pathways, the integrin signaling pathway, and T and B cell activation. Moreover, a change was identified in the expression of genes involved in both intercellular and intracellular signaling systems.

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