Key result
Angiotensin III stimulates ERK1/2 MAPK phosphorylation and DNA synthesis in vascular smooth muscle cells via AT1 receptors, though this effect is reduced in spontaneously hypertensive rats.
Why the study?
Although Ang II stimulates ERK1/2 and VSMC proliferation, whether Ang III induces ERK1/2 MAPK and proliferation in Wistar and SHR VSMCs remained to be explored.
Does Angiotensin III induce ERK1/2 MAPK phosphorylation and cellular proliferation in rat vascular smooth muscle cells?
Does Angiotensin III induce ERK1/2 MAPK phosphorylation and cellular proliferation in rat vascular smooth muscle cells?
Answers are grounded in this paper and cite their sources.
Angiotensin III stimulates ERK1/2 MAPK and DNA synthesis in vascular smooth muscle cells via AT1 receptors, with reduced effects in spontaneously hypertensive rats compared to normotensive rats.
The proliferative effects of angiotensin (Ang) II in vascular smooth muscle cells (VSMCs) through its ability to stimulate extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway have been established. The main goal of this study was to explore whether Ang III induces ERK1/2 MAPK and VSMC proliferation in cultured Wistar VSMCs. Further, the Ang III actions were compared to those observed in VSMCs derived from the spontaneously hypertensive rat (SHR). We hypothesized that in VSMCs Ang III will have similar actions as Ang II to induce ERK1/2 MAPK and cellular proliferation and this ability may be different in VSMCs isolated from Wistar versus SHR rats. Time and/or concentration-dependent effects of Ang III and Ang II were determined in VSMCs using western blot analysis and DNA incorporation assay. The results showed that ERK1/2 MAPK phosphorylation mediated by Ang II or Ang III were concentration- and time-dependent in Wistar VSMCs. Moreover, Ang III was less effective in mediating ERK1/2 phosphorylation in SHR VSMCs as compared to effects seen in Wistar rat VSMCs. Ang III induced ERK1/2 phosphorylation through the AT1 receptors activation. Ang II and Ang III induced VSMC DNA synthesis via the AT1 receptor in a concentration-dependent manner in Wistar VSMCs. Moreover, Ang III induced VSMC proliferation and significant differences existed in the peptide's proliferation effects in Wistar versus SHR VSMCs. These results indicate that Ang III stimulates ERK1/2 MAPK and DNA synthesis in VSMCs via AT1 receptors. However, its ability to stimulate these pathways is reduced in SHR VSMCs.
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Alanazi et al. (2025) studied this question. Angiotensin III vs. Angiotensin II / SHR vs Wistar VSMCs was evaluated on ERK1/2 MAPK phosphorylation and DNA synthesis. Angiotensin III stimulates ERK1/2 MAPK phosphorylation and DNA synthesis in vascular smooth muscle cells via AT1 receptors, though this effect is reduced in spontaneously hypertensive rats.
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