Moraes João Alfredo, Frony Ana Clara, Dias Aline Maria, Renovato-Martins Mariana, Rodrigues Genilson, Marcinkiewicz Cezary, Assreuy Jamil, Barja-Fidalgo Christina
Laboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, RJ, Brazil.
Department of Bioengineering, College of Engineering, Temple University, Philadelphia, PA, USA.
Data Brief. 2015 Dec 17;6:330-40. doi: 10.1016/j.dib.2015.11.053. eCollection 2016 Mar.
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.
这些数据为研究文章Moraes等人发表于《动脉粥样硬化》2015年第243卷第2期第477 - 485页的[1]提供了支持信息。在此，我们提供了血管紧张素II（Ang II）对血管平滑肌细胞（VSMC）作用机制背后的数据。Ang II诱导的VSMC活性氧（ROS）产生受α1β1整合素调节。Ang II还通过NOX2亚基p47（phox）刺激VSMC中的ROS产生。此外，NOX2抑制剂也抑制了Ang II对VSMC迁移的作用。我们发现钝抑素（一种α1β1整合素阻滞剂）抑制了Ang II对p47（phox）激活的作用。Ang II对ROS产生的作用也依赖于磷脂酰肌醇3 -激酶（PI3K）。最后，我们表明NOX1和整合素连接激酶（ILK）对NOX2激活至关重要。该研究提供了关于在Ang II对VSMC的作用中，NOX1/α1β1整合素/ILK/NOX2的一系列事件的信息。
