Abstract
The data provides information in support of the research article Moraes et al., Atherosclerosis 243(2) (2015) 477–485 [1]. Here we provide data behind the mechanisms involved in Angiotensin II (Ang II) effects on vascular smooth muscle cells (VSMC). Ang II-induced VSMC ROS production is modulated by alpha1beta1 integrin. Ang II also stimulates ROS production in VSMC via p47phox, a NOX2 subunit. Furthermore, Ang II effect on VSMC migration was also inhibited by NOX2 inhibitor. We showed that obtustatin, alpha1beta1 integrin blocker, inhibited Ang II effect on p47phox activation. Ang II effect on ROS production is also PI3K dependent. Finally we showed that NOX1 and Integrin-Linked-Kinase (ILK) are crucial to NOX2 activation. The research provides information about the sequential events of NOX1/alpha1beta1 integrin/ILK/NOX2 in Ang II effects on VSMC.
Highlights
Angiotensin II (Ang II) effect on vascular smooth muscle cells (VSMC) migration relies in NOX2 activity, once we observed that the pretreatment of VSMC with Apocynin inhibited the chemotactic effect of Ang II (Fig. 2)
It is well described that VSMC contains NOX2 [2,3], so we investigated the presence of this protein in the VSMC line A7r5
As we can observe through cytosol/membrane fraction analysis, Ang II was able to induce p47phox translocation to VSMC membrane 10 min after treatment (Fig. 5A)
Summary
Ang II effect on VSMC migration relies in NOX2 activity, once we observed that the pretreatment of VSMC with Apocynin inhibited the chemotactic effect of Ang II (Fig. 2). It is well described that VSMC contains NOX2 [2,3], so we investigated the presence of this protein in the VSMC line A7r5. P47phox and alpha1beta integrin modulate angiotensin II effect on NOX2 activation in VSMC. When p47phox interacts with the NOX2 membrane subunit, NOX2 becomes a full complex and it is ready to initiate ROS production [4,5].
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