Apolipoprotein E-deficient male and female mice (aged 7 wk; n = 25 per group) were infused with angiotensin II (AngII; 2000 ng/kg/min) plus β-aminopropionitrile (BAPN) in the drinking water for 28 d to test the effects of gender on AAA rupture.
Apolipoprotein E-deficient male and female mice (aged 7 wk; n = 25 per group) were infused with angiotensin II (AngII; 2000 ng/kg/min) plus β-aminopropionitrile (BAPN) in the drinking water for 28 d to test the effects of gender on AAA rupture.
CD11c+ depletion commencing after AAA establishment by 14 days of AngII infusion, was also shown to lead to smaller AAAs than controls after a further 14 days (D.tox, 1.54 ± 0.04 mm vs Vehicle control, 1.80 ± 0.03 mm, P<0.001).
The effect of conditional depletion of CD11c+ cells on experimental AAA was investigated in the angiotensin II (AngII)-infused apolipoprotein E-deficient (ApoE-/-) mouse model.
CD11c+ depletion commencing after AAA establishment by 14 days of AngII infusion, was also shown to lead to smaller AAAs than controls after a further 14 days (D.tox, 1.54 ± 0.04 mm vs Vehicle control, 1.80 ± 0.03 mm, P<0.001).
Here we report a pathogenic role for the interleukin-27 receptor (IL-27R) in AAA, as genetic ablation of IL-27R protects mice from the disease development.
Here we report a pathogenic role for the interleukin-27 receptor (IL-27R) in AAA, as genetic ablation of IL-27R protects mice from the disease development.
Here, we investigated the gene regulatory function for one of four non-coding SNPs associated with AAA, rs2836411, which is located in an intron of the ERG gene.
A recently published genome wide association study of abdominal aortic aneurysms (AAA), based on pooled case control data of European ancestry, identified four new loci for AAA: SMYD2 (top single nucleotide polymorphism [SNP] rs1795061), LINC00540 (rs9316871), PCIF1/MMP9/ZNF335 (rs3827066), and ERG (rs2836411).
A recently published genome wide association study of abdominal aortic aneurysms (AAA), based on pooled case control data of European ancestry, identified four new loci for AAA: SMYD2 (top single nucleotide polymorphism [SNP] rs1795061), LINC00540 (rs9316871), PCIF1/MMP9/ZNF335 (rs3827066), and ERG (rs2836411).
A recently published genome wide association study of abdominal aortic aneurysms (AAA), based on pooled case control data of European ancestry, identified four new loci for AAA: SMYD2 (top single nucleotide polymorphism [SNP] rs1795061), LINC00540 (rs9316871), PCIF1/MMP9/ZNF335 (rs3827066), and ERG (rs2836411).
A recently published genome wide association study of abdominal aortic aneurysms (AAA), based on pooled case control data of European ancestry, identified four new loci for AAA: SMYD2 (top single nucleotide polymorphism [SNP] rs1795061), LINC00540 (rs9316871), PCIF1/MMP9/ZNF335 (rs3827066), and ERG (rs2836411).
A recently published genome wide association study of abdominal aortic aneurysms (AAA), based on pooled case control data of European ancestry, identified four new loci for AAA: SMYD2 (top single nucleotide polymorphism [SNP] rs1795061), LINC00540 (rs9316871), PCIF1/MMP9/ZNF335 (rs3827066), and ERG (rs2836411).
In the in vivo experiment, Ang-(1-7) treatment reduced the incidence and severity of AAA induced by Ang II infusion, and the mechanisms involved inhibited macrophage infiltration, attenuated expression of interleukin 6(IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein 1(MCP-1) and matrix metalloprotease 2(MMP2), as well as abated SMCs apoptosis in the abdominal aortic tissues.
In the in vivo experiment, Ang-(1-7) treatment reduced the incidence and severity of AAA induced by Ang II infusion, and the mechanisms involved inhibited macrophage infiltration, attenuated expression of interleukin 6(IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein 1(MCP-1) and matrix metalloprotease 2(MMP2), as well as abated SMCs apoptosis in the abdominal aortic tissues.
In the in vivo experiment, Ang-(1-7) treatment reduced the incidence and severity of AAA induced by Ang II infusion, and the mechanisms involved inhibited macrophage infiltration, attenuated expression of interleukin 6(IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein 1(MCP-1) and matrix metalloprotease 2(MMP2), as well as abated SMCs apoptosis in the abdominal aortic tissues.
In the in vivo experiment, Ang-(1-7) treatment reduced the incidence and severity of AAA induced by Ang II infusion, and the mechanisms involved inhibited macrophage infiltration, attenuated expression of interleukin 6(IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein 1(MCP-1) and matrix metalloprotease 2(MMP2), as well as abated SMCs apoptosis in the abdominal aortic tissues.
In the present study, we collected clinical AAA specimens and constructed AAA mice model through Ang-II infusion, and found apparently increased MCPIP1 expression and severe inflammatory infiltration in AAA aortic membrane as evidenced by elevated levels of monocyte chemotactic protein 1 (MCP-1), interleukin 1 β (IL-1β) and NF-κB, as well as HE staining.