Mechanism of Angiotensin II-induced Superoxide Production in Cells Reconstituted with Angiotensin Type 1 Receptor and the Components of NADPH Oxidase

Choi, Han Seok; Leto, Thomas L.; Hunyady, László; Catt, Kevin J.; Bae, Yun Soo; Rhee, Sue Goo

doi:10.1074/jbc.m708000200

Cited by 59 publications

(47 citation statements)

References 93 publications

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“…In the presence of the flavoenzyme Nox inhibitor DPI, AngII stimulation of cofilin dephosphorylation was blocked, indicating the requirement for ROS formation in this process ( Figure 4B). Similarly wortmannin, an inhibitor of the downstream mediator of AngII signaling to Nox1, PI 3-kinase (Choi et al, 2008), also blocked cofilin dephosphorylation ( Figure 4B). Consistent with our earlier results using H 2 O 2 , the overexpression of 14-3-3-wt inhibited cofilin activation compared with control cells, whereas the nonbinding 14-3-3-K49E mutant had no inhibitory effect in AngII-stimulated HeLa cells ( Figure 4C).…”

Section: Angii-induced Ros Generation Activates Cofilinmentioning

confidence: 99%

Reactive Oxygen Species Regulate a Slingshot-Cofilin Activation Pathway

Kim

Huang

Bokoch

2009

MBoC

177

163

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Cellular stimuli generate reactive oxygen species (ROS) via the local action of NADPH oxidases (Nox) to modulate cytoskeletal organization and cell migration through unknown mechanisms. Cofilin is a major regulator of cellular actin dynamics whose activity is controlled by phosphorylation/dephosphorylation at Ser3. Here we show that Slingshot-1L (SSH-1L), a selective cofilin regulatory phosphatase, is involved in H 2 O 2 -induced cofilin dephosphorylation and activation. SSH-1L is activated by its release from a regulatory complex with 14-3-3 protein through the redox-mediated oxidation of 14-3-3 by H 2 O 2 . The ROS-dependent activation of the SSH-1L-cofilin pathway stimulates the SSH-1L-dependent formation of cofilin-actin rods in cofilin-GFP-expressing HeLa cells. Similarly, the formation of endogenous ROS stimulated by angiotensin II (AngII) also activates the SSH-1L-cofilin pathway via oxidation of 14-3-3 to increase AngII-induced membrane ruffling and cell motility. These results suggest that the formation of ROS by NADPH oxidases engages a SSH-1L-cofilin pathway to regulate cytoskeletal organization and cell migration.

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Section: Angii-induced Ros Generation Activates Cofilinmentioning

confidence: 99%

Reactive Oxygen Species Regulate a Slingshot-Cofilin Activation Pathway

Kim

Huang

Bokoch

2009

MBoC

177

163

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“…AT1R activation triggers multiple assembly and activation of G-proteins (including Gaq, Gbg). The further downstream signals from AT1R include Rac activation via PI 3-kinase activation and PKC activation which causes p47phox phosphorylation [62]. Rac activation and p47phox phosphorylation enable the multimer recruitment and assembly of the active form of NADPH oxidase.…”

Section: Signalling Pathway Under Circumferential Stretch In Endothelmentioning

confidence: 99%

Role of shear stress and stretch in vascular mechanobiology

Kassab

2011

J. R. Soc. Interface.

272

198

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Blood vessels are under constant mechanical loading from blood pressure and flow which cause internal stresses (endothelial shear stress and circumferential wall stress, respectively). The mechanical forces not only cause morphological changes of endothelium and blood vessel wall, but also trigger biochemical and biological events. There is considerable evidence that physiologic stresses and strains (stretch) exert vasoprotective roles via nitric oxide and provide a homeostatic oxidative balance. A perturbation of tissue stresses and strains can disturb biochemical homeostasis and lead to vascular remodelling and possible dysfunction (e.g. altered vasorelaxation, tone, stiffness, etc.). These distinct biological endpoints are caused by some common biochemical pathways. The focus of this brief review is to point out some possible commonalities in the molecular pathways in response to endothelial shear stress and circumferential wall stretch.

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“…In the renin transgenic rat, with high circulating Ang II, oxidative stress was attenuated by statin treatment resulting in less podocyte damage. 37 In addition to their cholesterol-lowering effects, statins also inhibit Rac1 and Nox-dependent O 2 Ϫ . In a model of slowly developing hypertension created by infusion of a low dose of Ang II, mice deficient of extracellular SOD (EC-SOD) had similar increases in MAP compared with wild-type mice.…”

Section: Ang Ii-o 2 ؊ In the Kidneymentioning

confidence: 99%

“…Nox1 and Nox2, as well as isoforms of p47 phox and p67 phox , NoxO1, and NoxA1 were transfected into cultured human embryonic kidney (HEK293) cells before Ang II exposure. Ang II increased activity of both Nox1 and Nox2, which was linked to intermediates G␣(q/11), phospholipase C-␤, and protein kinase C. 2 Maximal activity of Nox1 required NoxO1 and NoxA1, and Nox2 required p47 phox and p67 phox . Ang II effects on Nox2 were more predominant and required additional pathways, including phosphatidylinositol 3-kinase and Rac1, which confirms earlier studies.…”

mentioning

confidence: 99%

Angiotensin II–Dependent Superoxide

Welch

2008

Hypertension

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A ngiotensin (Ang) II generates reactive oxygen species (ROS) by activation of Ang II type 1 receptors (AT 1 Rs). The resulting ROS mediates many of the actions of Ang II, including constriction of vascular smooth muscles, increased systemic blood pressure (BP), endothelial dysfunction, vascular remodeling, and sodium retention. Ang II has its greatest effect on superoxide anion (O 2 Ϫ ), which may be an important signaling element of the hypertensive rats and other deleterious actions of Ang II. The mechanisms of ROS actions are not fully understood, yet effective antioxidant therapy often attenuates hypertension and other vascular effects of Ang II. Currently many studies use Ang II-infused animal models to investigate the role of ROS and interacting systems, not only on hypertension, but endothelial dysfunction, renal disease, heart disease, and other pathologies. This review focuses on the recent reports of Ang II-generated ROS and how it impacts hypertension and its vascular consequences.

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Mechanism of Angiotensin II-induced Superoxide Production in Cells Reconstituted with Angiotensin Type 1 Receptor and the Components of NADPH Oxidase

Cited by 59 publications

References 93 publications

Reactive Oxygen Species Regulate a Slingshot-Cofilin Activation Pathway

Reactive Oxygen Species Regulate a Slingshot-Cofilin Activation Pathway

Role of shear stress and stretch in vascular mechanobiology

Angiotensin II–Dependent Superoxide

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