Key result
Binding of prorenin to the (pro)renin receptor induces human umbilical artery smooth muscle cell proliferation via ROS generation and ERK1/2 activation independently of AngII.
Prorenin induces proliferation of human umbilical artery smooth muscle cells via ROS generation and ERK1/2 activation, highlighting an AngII-independent pathway of the renin-angiotensin system.
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Does not change clinical practice; leaves open whether (pro)renin receptor targeting adds benefit beyond AngII blockade in vascular disease.
INTRODUCTION: Since the discovery of the (pro)renin receptor (PRR), it has been considered as a novel bioactive molecule of the renin-angiotensin system (RAS). The activation of PRR can elicit a series of angiotensin II (AngII)-independent effects. MATERIALS AND METHODS: In this study, we investigated the effects of prorenin and PRR on the proliferation of human umbilical artery smooth muscle (HUASM) cells and explored the possible mechanisms underlying these effects. RESULTS: The binding of prorenin to PRR can promote proliferation and upregulate the anti-apoptotic protein Bcl-2 and downregulate the pro-apoptotic protein Bax independently of AngII in HUASM cells. In addition, the binding of prorenin to PRR can also increase the production of reactive oxygen species (ROS) and the phosphorylation of extracellular signal-regulated kinase (ERK1/2) independently of AngII. The pretreatment of HUASM cells with an NADPH oxidase inhibitor DPI decreased the production of ROS and also decreased the phosphorylation of ERK1/2. Furthermore, pretreatment of HUASM cells with DPI and the ERK1/2 inhibitor PD98059 significantly attenuated the prorenin-induced proliferation and regulation of apoptosis factors. CONCLUSION: Binding of prorenin to PRR can induce HUASM cell proliferation via the ROS generation and ERK1/2 activation.
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Liu et al. (2014) studied this question. Prorenin was evaluated on Proliferation of human umbilical artery smooth muscle (HUASM) cells. Binding of prorenin to the (pro)renin receptor induces human umbilical artery smooth muscle cell proliferation via ROS generation and ERK1/2 activation independently of AngII.
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