scholarly journals Modulating Neuro-Immune-Induced Macrophage Polarization With Topiramate Attenuates Experimental Abdominal Aortic Aneurysm

2020 ◽  
Vol 11 ◽  
Author(s):  
Xing Chen ◽  
Yang Li ◽  
Jie Xiao ◽  
Hua Zhang ◽  
Chuanlei Yang ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Macrophage Polarization ◽  
Abdominal Aortic

scholarly journals Eosinophils Protect Mice from Angiotensin-II Perfusion-Induced Abdominal Aortic Aneurysm

2020 ◽  
Author(s):  
Cong-Lin Liu ◽  
Xin Liu ◽  
Yuanyuan Zhang ◽  
Jing Liu ◽  
Chongzhe Yang ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Macrophage Polarization ◽  
Aortic Disease ◽  
Immunofluorescent Staining ◽  
Blood Eosinophil ◽  
Cationic Protein ◽  
Abdominal Aortic ◽  
M1 Macrophage

Rationale: Blood eosinophil (EOS) count and EOS cationic protein (ECP) associate with human cardiovascular diseases (CVD). Yet, whether EOS play a role in CVD remains untested. The current study detected EOS accumulation in human and murine abdominal aortic aneurysm (AAA) lesions, suggesting EOS participation in this aortic disease. Objective: To test whether and how EOS affect AAA growth. Methods and Results: Population-based randomized clinically controlled screening trials revealed higher blood EOS count in 579 male AAA patients than in 5,063 non-AAA control (0.236{plus minus}0.182 vs 0.211{plus minus}0.154, 109/L, P<0.001). Univariate (OR=1.381, P<0.001) and multivariate (OR=1.237, P=0.031) logistic regression analyses indicated that increased blood EOS count in AAA patients served as an independent risk factor of human AAA. Immunostaining and immunoblot analyses detected EOS accumulation and EOS cationic protein expression in human and murine AAA lesions. Results showed that EOS deficiency exacerbated AAA growth with increased lesion inflammatory cell contents, matrix-degrading protease activity, angiogenesis, cell proliferation and apoptosis, and smooth muscle cell (SMC) loss using angiotensin-II perfusion-induced AAA in Apoe -/- and EOS-deficient Apoe -/- ;∆dblGATA mice. EOS deficiency increased lesion chemokine expression, muted lesion expression of IL4 and EOS-associated-ribonuclease-1 (mEar1, human ECP homolog), and slanted M1 macrophage polarization. In cultured macrophages and monocytes, EOS-derived IL4 and mEar1 polarized M2 macrophages, suppressed CD11b+Ly6Chi monocytes, and increased CD11b + Ly6C lo monocytes. mEar1 treatment or adoptive transfer of EOS from WT and Il13 -/- mice, but not EOS from Il4 -/- mice, blocked AAA growth in Apoe -/- ∆dblGATA mice. Immunofluorescent staining and immunoblot analyses demonstrated a role for EOS IL4 and mEar1 in blocking NF-κB activation in macrophages, SMCs, and endothelial cells. Conclusions: EOS play a protective role in AAA by releasing IL4 and cationic proteins such as mEar1 to regulate macrophage and monocyte polarization and to block NF-κB activation in aortic inflammatory and vascular cells.

scholarly journals Elastin-Derived Peptides Promote Abdominal Aortic Aneurysm Formation by Modulating M1/M2 Macrophage Polarization

2016 ◽  
Vol 196 (11) ◽  
pp. 4536-4543 ◽  
Author(s):  
Matthew A. Dale ◽  
Wanfen Xiong ◽  
Jeffrey S. Carson ◽  
Melissa K. Suh ◽  
Andrew D. Karpisek ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
M2 Macrophage Polarization

scholarly journals D‐series resolvins inhibit murine abdominal aortic aneurysm formation and increase M2 macrophage polarization

2016 ◽  
Vol 30 (12) ◽  
pp. 4192-4201 ◽  
Author(s):  
Nicolas H. Pope ◽  
Morgan Salmon ◽  
John P. Davis ◽  
Anuran Chatterjee ◽  
Gang Su ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Aneurysm Formation ◽  
Abdominal Aortic ◽  
M2 Macrophage Polarization

Hemoglobin induces monocyte recruitment and CD163-macrophage polarization in abdominal aortic aneurysm

2015 ◽  
Vol 201 ◽  
pp. 66-78 ◽  
Author(s):  
Alfonso Rubio-Navarro ◽  
Juan Manuel Amaro Villalobos ◽  
Jes S. Lindholt ◽  
Irene Buendía ◽  
Jesús Egido ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Macrophage Polarization ◽  
Abdominal Aortic ◽  
Monocyte Recruitment

Abstract 492: Resolvin D2 Inhibits Murine Abdominal Aortic Aneurysm and Increases M2 Macrophage Differentiation

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Nicolas H Pope ◽  
Morgan Salmon ◽  
Michael S Conte ◽  
Gorav Ailawadi ◽  
Gilbert R Upchurch
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Inflammatory Cytokines ◽  
Macrophage Polarization ◽  
Neointimal Hyperplasia ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
Cytokine Analysis ◽  
Abdominal Aortic ◽  
Pro Inflammatory Cytokines

Objectives: Macrophages are critical to abdominal aortic aneurysm (AAA) formation; however, the role of anti-inflammatory M2 macrophages is not known. Resolvins have been shown to play a protective role in neointimal hyperplasia; however, their role in AAA has not been established. We hypothesized that treatment with Resolvin D2 (RvD2) attenuates murine AAA formation through alterations in macrophage polarization and cytokine expression. Methods: Male C57/B6 mice (n=9/group) of 8-12 weeks of age received RvD2 (100 ng/kg/treatment) or vehicle only every third day beginning three days prior to abdominal aortic perfusion with elastase. Aortas were harvested 14 days following elastase perfusion. Cytokine analysis (n=5/group) or confocal microscopy (n=4/group) was performed. Cytokine profiles were analyzed using a murine antibody array. To determine the effect of RvD2 on macrophage polarization, confocal staining for macrophages (Mac2), M1 (MCP-1) and M2 (Arg-1) macrophage subtypes, α-actin and 4',6-diamidino-2-phenylindole (DAPI) was utilized. Results: Mean aortic dilation was 96.23 % (± 13.07 %) for vehicle treated and 56.58% (± 9.69%) for RvD2 treated mice (p<0.0001). Pro-inflammatory cytokines CXCL-10, IL-1β, TIMP-1 and MCP-1 were significantly elevated in control as compared to RvD2 treated animals. Confocal histology demonstrated a prevalence of M2 macrophages within the aortic media in mice treated with RvD2 (Figure 1). Conclusions: Resolvin D2 exhibits a potent protective effect against experimental AAA formation. Treatment with RvD2 significantly influences macrophage polarization and decreases several important pro-inflammatory cytokines. Resolvins and the alteration of macrophage polarization represent potential future targets for prevention of AAA.

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