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Abstract
The aim of the present study was to identify abdominal aortic aneurysms (AAA)-associated miR-155 contributing to AAA pathology by regulating macrophage-mediated inflammation. Angiotensin II (AngII)–infused apolipoprotein E-deficient (ApoE-/-) mice and THP-1 cells model of miR-155 overexpression and deficiency were used in the experiments. The expression of miR-155 was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cytokines were evaluated using enzyme-linked immunoabsorbent assay (ELISA). Western blotting was used to measure the levels of MMP-2, MMP-9, iNOS, and monocyte chemoattractant protein (MCP)-1 proteins. Immunostaining and transwell were used to determine CD68, elastic collagen, proliferation, and migration of vascular smooth muscle cells (VSMCs). The results showed that miR-155 and cytokines were up-regulated in AAA patients or ApoE-/- mice. Overexpression of miR-155 enhanced MMP-2, MMP-9, iNOS, and MCP-1 levels, and stimulated the proliferation and migration of VSMCs. Meanwhile, inhibition of miR-155 had the opposite effect. In addition, histology demonstrated accumulation of CD68 and elastic collagen-positive areas significantly decreased in miR-155 antagomir injection group. In conclusion, the results of the present study suggest that inhibiting miR-155 is crucial to prevent the development of AAA by regulating macrophage inflammation.
Highlights
enzyme-linked immunoabsorbent assay (ELISA) was performed to assess the effect of Abdominal aortic aneurysms (AAA) on inflammation in serum of Angiotensin II (AngII)–infused apolipoprotein E-deficient (ApoE-/-)mice
The results showed that tumor necrosis factor-alpha (TNFα), IL-6, and interleukin-1 beta (IL-1β) levels were significantly increased as compared with the control groups (P
AAA is a serious late onset vascular disease with high mortality. miR-155 may play a role in AAA pathology based on influence of its overexpression and deficiency exist on inflammatory factors [45,46]
Summary
Abdominal aortic aneurysms (AAA) are defined as focal dilatation of the abdominal aorta when it is 50% greater than its normal diameter or when it is more than 3 cm in the abdominal aorta diameter. AAA is a common disease with an irreversible dilatation of the abdominal aorta, which is characterized by high mortality and asymptomatic [1]. Macrophages in AAA formation and rupture have significant effect [7]. The pathogenesis probably occurs with the injury of endothelial and vascular smooth muscle cells (VSMCs), which recruits an inflammatory response to lead to destroy the integrity c 2018 The Author(s).
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