Genotyping of rs1024611 in the MCP-1 gene was performed using TaqMan predesigned SNP genotyping assays in 27 patients with AAA (63% men, mean age of 71).
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.
In vivo overexpression of H19 increased vascular inflammation and induced AAA formation, which was supported by exacerbated aortic morphology, maximum aortic diameter values, elastin degradation, expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1), and macrophage infiltration.
Levo-Tetrahydropalmatine Attenuates Progression of Abdominal Aortic Aneurysm in an Elastase Perfusion Rat Model via Suppression of Matrix Metalloproteinase and Monocyte Chemotactic Protein-1.
Reduced macrophage accumulation and monocyte chemotactic protein-1 expression were observed in calcium chloride-induced AAA walls in miR-33<sup>-/-</sup> mice.
In addition, the protein expressions of several key components involved in AAA pathogenic features are as follows: matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of matrix metalloproteinase (TIMP)-1 and TIMP-2 for elastin degradation; collagen type 1 alpha 1 for compensatory collagen synthesis; monocyte chemoattractant protein-1 for inflammation, were also evaluated.
RELMβ gene deficiency significantly decreased AAA incidence and severity, which was associated with reduced macrophage accumulation and decreased expression of proinflammatory cytokines (monocyte chemoattractant protein 1 and interleukin 6), matrix metalloproteinase 2 (MMP-2) and MMP-9 in the aortic wall.
In vitro study showed that treating VSMCs with TNF-α together with DOX remarkably inhibited the expressions and activities of MMPs (MMP-2 and MMP-9), significantly suppressed the activation of protein kinase B (AKT) signaling pathway and mitogen-activated protein kinases (MAPKs) signal proteins, including extracellular signal-regulated kinase (ERK), c-Jun amino-terminal kinases (JNK) and p38, and downregulated mRNA levels of interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1), and significantly upregulated mRNA levels of transforming growth factor beta (TGF-β), heme oxygenase 1 (HO-1) and superoxide dismutase 1 (SOD-1), indicating that DOX inhibits activities of MMPs through reducing oxidative stress, suppressing MAPKs and AKT signaling pathways and ameliorating inflammation in VSMCs, and therefore, exerts preventive as well as therapeutic effects on AAA.
Increased levels of proinflammatory interleukin-6 and monocyte chemoattractant protein-1 were preferentially colocalized within adventitial fibroblasts in HHcy plus angiotensin II mice, which suggested the importance of adventitial fibroblasts activation in Hcy-aggravated AAA.
Under these conditions, the gene expressions of monocyte chemotactic protein-1 and its receptor, CCR-2, were not significantly different in the control and diseased regions of both AAA and CAS.