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

João Alfredo Moraes; Ana Clara Frony; Aline Maria Dias; Mariana Renovato-Martins; Genilson Rodrigues; Cezary Marcinkiewicz; Jamil Assreuy; Christina Barja-Fidalgo

doi:10.1016/j.dib.2015.11.053

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

Data Brief. 2015 Dec 17:6:330-40. doi: 10.1016/j.dib.2015.11.053. eCollection 2016 Mar.

Authors

João Alfredo Moraes¹, Ana Clara Frony¹, Aline Maria Dias¹, Mariana Renovato-Martins¹, Genilson Rodrigues¹, Cezary Marcinkiewicz², Jamil Assreuy³, Christina Barja-Fidalgo¹

Affiliations

¹ Laboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, RJ, Brazil.
² Department of Bioengineering, College of Engineering, Temple University, Philadelphia, PA, USA.
³ Department of Pharmacology, Universidade Federal de Santa Catarina (UFSC), Florianópolis, SC, Brazil.

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 p47 (phox) , 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 p47 (phox) 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.