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- W2132193621 abstract "Inflammation is a key event in the development of atherosclerosis. Nuclear factor-κB (NF-κB) is important in the inflammatory response regulation. The effector peptide of the renin angiotensin system Angiotensin II (Ang II) activates NF-κB and upregulates some related proinflammatory genes. Our aim was to investigate whether other angiotensin-related peptides, as the N-terminal degradation peptide Ang IV, could regulate proinflammatory factors (activation of NF-κB and related genes) in cultured vascular smooth muscle cells (VSMCs). In these cells, Ang IV increased NF-κB DNA binding activity, caused nuclear translocation of p50/p65 subunits, cytosolic IκB degradation and induced NF-κB–dependent gene transcription. Ang II activates NF-κB via AT 1 and AT 2 receptors, but AT 1 or AT 2 antagonists did not inhibit NF-κB activation caused by Ang IV. In VSMC from AT 1a receptor knockout mice, Ang IV also activated NF-κB pathway. In those cells, the AT 4 antagonist divalinal diminished dose-dependently Ang IV–induced NF-κB activation and prevented IκB degradation, but had no effect on the Ang II response, indicating that Ang IV activates the NF-κB pathway via AT 4 receptors. Ang IV also increased the expression of proinflammatory factors under NF-κB control, such as MCP-1, IL-6, TNF-α, ICAM-1, and PAI-1, which were blocked by the AT 4 antagonist. Our results reveal that Ang IV, via AT 4 receptors, activates NF-κB pathway and increases proinflammatory genes. These data indicate that Ang IV possesses proinflammatory properties, suggesting that this Ang degradation peptide could participate in the pathogenesis of cardiovascular diseases." @default.
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- W2132193621 date "2005-05-13" @default.
- W2132193621 modified "2023-10-18" @default.
- W2132193621 title "Angiotensin IV Activates the Nuclear Transcription Factor-κB and Related Proinflammatory Genes in Vascular Smooth Muscle Cells" @default.
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- W2132193621 doi "https://doi.org/10.1161/01.res.0000166326.91395.74" @default.
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