Data in support of alpha1beta1 and integrin-linked kinase interact and modulate angiotensin II effects in vascular smooth muscle cells

• Published in: Data in brief Vol. 6; pp. 330 - 340
• Main Authors: Moraes, João Alfredo, Frony, Ana Clara, Dias, Aline Maria, Renovato-Martins, Mariana, Rodrigues, Genilson, Marcinkiewicz, Cezary, Assreuy, Jamil, Barja-Fidalgo, Christina
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01-03-2016; Elsevier
• Subjects: Data
• ISSN: 2352-3409; 2352-3409
• DOI: 10.1016/j.dib.2015.11.053

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.