Angiotensin II-mediated expression of p27Kip1 and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals

Hannken, Tete; Schroeder, Regine; Stahl, Rolf A.K.; Wolf, Günter

doi:10.1046/j.1523-1755.1998.00212.x

Cited by 157 publications

(124 citation statements)

References 41 publications

(69 reference statements)

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“…Our previous findings (19) suggest that this downregulation of Mn-SOD with salt loading may be a consequence of a reduction in Ang II, but this was not tested in the present study. ROS activate mitogen-activated protein kinase in renal tubule cells (38), contribute to hypertrophic responses to Ang II (38) and to cellular injury (39), and increase fibrogenic matrix protein synthesis in mesangial cells (40). A high salt intake enhances oxidative stress in rat skeletal muscle arterioles and vessels (23) and increases BP, protein excretion, and renal fibrosis and worsens renal function in several models of chronic renal failure (7,38,(41)(42)(43) and accelerates the decline of renal function in patients with chronic renal failure (44).…”

Section: Discussionmentioning

confidence: 99%

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Kitiyakara

Chabrashvili²,

Chen³

et al. 2003

Journal of the American Society of Nephrology

281

236

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Abstract. The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and was related to renal cortical expression of NAD(P)H oxidase and superoxide dismutase (SOD). 8-Isoprostane PGF 2␣ and malonyldialdehyde were measured in groups (n ϭ 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH-and NADH-stimulated superoxide anion (O 2 ·Ϫ ) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-isoprostane and malonyldialdehyde increased incrementally twoto threefold with salt intake (P Ͻ 0.001), whereas prostaglandin E 2 was unchanged. Renal cortical NADH-and NADPHstimulable O 2 ·Ϫ generation increased (P Ͻ 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P Ͻ 0.005) increased renal cortical mRNA expression of gp91 phox and p47 phox and decreased expression of intracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD. Despite suppression of the renin-angiotensin system, salt loading enhances oxidative stress. This is accompanied by increased renal cortical NADH and NADPH oxidase activity and increased expression of gp91 phox and p47 phox and decreased IC-and Mn-SOD. Thus, salt intake enhances generation of O 2 ·Ϫ accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC-and Mn-SOD.

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Section: Discussionmentioning

confidence: 99%

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Kitiyakara

Chabrashvili²,

Chen³

et al. 2003

Journal of the American Society of Nephrology

281

236

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“…In mesangial cells, NO inhibits the expression of Nox1, suggesting cross-talk between NO and O 2 иϪ -generating systems (244). p22 phox , p47 phox , and p67 phox are all expressed in the PCT, DCT, CCD, and the macula densa cells (12,72,107,…”

Section: Nistala Et Al 2060mentioning

confidence: 99%

Redox Control of Renal Function and Hypertension

Nistala

Whaley‐Connell

Sowers

2008

Antioxidants & Redox Signaling

138

123

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“…On the other hand, the cell cycle molecular machinery has also been implicated to play an important role in cellular hypertrophy in VSMCs and IRPTCs (40,(67)(68)(69). Cell cycle entry and progression, the final common pathway of cell-growth response, depends on the carefully regulated expression and ac- tivation of certain proteins, termed cyclin-dependent kinases (ckd), and their regulatory subunits, the cyclins (40,70).…”

Section: Hypertrophic Effects Of the Glp Gene In Irptcs-irptcsmentioning

confidence: 99%

A Novel Angiotensin II Type 1 Receptor-associated Protein Induces Cellular Hypertrophy in Rat Vascular Smooth Muscle and Renal Proximal Tubular Cells

Guo

Tardif

Ghelima

et al. 2004

Journal of Biological Chemistry

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Angiotensin II stimulates cellular hypertrophy in cultured vascular smooth muscle and renal proximal tubular cells. This effect is believed to be one of earliest morphological changes of heart and renal failure. However, the precise molecular mechanism involved in angiotensin II-induced hypertrophy is poorly understood. In the present study we report the isolation of a novel angiotensin II type 1 receptor-associated protein. Angiotensin II (Ang II) 1 elicits a wide range of physiological responses in a variety of cell types. This octapeptide hormone plays an important role in the regulation of cardiovascular and renal functions via diverse mechanisms (1), which include arteriolar vasoconstriction, stimulation of aldosterone production, and electrolyte homeostasis (2). Although its vasoactive effects were initially considered to be a unique feature for maintaining blood pressure, recent studies have demonstrated that Ang II exerts many other important actions on the cardiovascular and renal systems. For example, Ang II stimulates the growth of diverse cell types, such as vascular smooth muscle cells (VSMC), cardiac myocytes, and proximal tubular cells (3-6), and it increases the expression of enzymes that produce mediators of inflammation (7,8). These observations suggest that Ang II may play an important role in various cardiovascular and renal diseases associated with abnormal cell growth (cellular hypertrophy or cell proliferation) and inflammation, such as hypertension, congestive heart failure, atherosclerosis, postangioplastic restenosis, and renal failure. Clinical trials and animal studies demonstrated that angiotensin-converting enzyme inhibitors and Ang II receptor blockers prevented vascular, left ventricular, and renal proximal tubular cellular hypertrophy (9 -13), supporting the importance of Ang II in the pathogenesis of cardiovascular and renal diseases. In vitro, Ang II has also been shown to stimulate the growth of VSMC and renal proximal tubular cells (hypertrophic effect) as well as cardiac myocytes and fibroblasts (hyperplastic action) (14 -17).

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Angiotensin II-mediated expression of p27Kip1 and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals

Cited by 157 publications

References 41 publications

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Redox Control of Renal Function and Hypertension

A Novel Angiotensin II Type 1 Receptor-associated Protein Induces Cellular Hypertrophy in Rat Vascular Smooth Muscle and Renal Proximal Tubular Cells

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