Role of Angiotensin II in the Transforming Growth Factor-.BETA.1 Expression of Rat Kidney in Anti-Glomerular Basement Membrane Antiserum-Induced Glomerulonephritis.

Yayama, Katsutoshi; Makino, Junko; Takano, Masaoki; Okamoto, Hiroshi

doi:10.1248/bpb.18.687

Cited by 14 publications

(6 citation statements)

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“…Our observation that blockade of the renin-angiotensin system with an AT 1 receptor antagonist can attenuate the enhanced TGF-␤, PAI-1, and matrix protein expression in renal disease is consistent with previous reports in a number of models of renal disease including partial nephrectomy (Junaid et al, 1997;Wu et al, 1997;Ali et al, 1998;Noda et al, 1999;Taal et al, 2001), immune-mediated renal injury (Yayama et al, 1995;Hisada et al, 1999), mesangioproliferative glomerulonephritis Zoja et al, 1998;Peters et al, 2000), hypertension-induced renal disease Otsuka et al, 1998;Wolf et al, 1998), unilateral ureteral obstruction (Ishidoya et al, 1995), cyclosporine nephrotoxicity (Shihab et al, 1997), and the diabetic transgenic (mRen-2)27 rat (Kelly et al, 2000).…”

Section: Discussionsupporting

confidence: 92%

The Angiotensin Type 1 Receptor Antagonist, Eprosartan, Attenuates the Progression of Renal Disease in Spontaneously Hypertensive Stroke-Prone Rats with Accelerated Hypertension

Abrahamsen

Barone²,

Campbell³

et al. 2002

J Pharmacol Exp Ther

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The effects of the angiotensin type 1 (AT 1 ) receptor antagonist, eprosartan, were studied in a model of severe, chronic hypertension. Treatment of male spontaneously hypertensive stroke prone rats (SHR-SP) fed a high-fat, high-salt diet with eprosartan (60 mg/kg/day i.p.) for 12 weeks resulted in a lowering of blood pressure (250 Ϯ 9 versus 284 Ϯ 8 mm Hg), renal expression of transforming growth factor-␤ mRNA (1.5 Ϯ 0.2 versus 5.4 Ϯ 1.4) and the matrix components: plasminogen activator inhibitor-1 (5.2 Ϯ 1.4 versus 31.4 Ϯ 10.7), fibronectin (2.2 Ϯ 0.6 versus 8.2 Ϯ 2.2), collagen I-␣1 (5.6 Ϯ 2.0 versus 23.8 Ϯ 7.3), and collagen III (2.7 Ϯ 0.9 versus 7.6 Ϯ 2.1). Data were corrected for rpL32 mRNA expression and expressed relative to Wistar Kyoto (WKY) rats [ϭ1.0]. Expression of fibronectin protein was also lowered by eprosartan (0.8 Ϯ 0.1 versus 1.9 Ϯ 0.5), relative to WKY rats. Eprosartan provided significant renoprotection to SHR-SP rats as measured by decreased proteinuria (22 Ϯ 2 versus 127 Ϯ 13 mg/day) and histological evidence of active renal damage (5 Ϯ 2 versus 195 Ϯ 6) and renal fibrosis (5.9 Ϯ 0.7 versus 16.4 Ϯ 1.9) in vehicle-versus eprosartantreated rats, respectively. Our results demonstrated that AT 1 receptor blockade with eprosartan can reduce blood pressure and preserve renal structure and function in this model of severe, chronic hypertension. These effects were accompanied by a decreased renal expression of transforming growth factor-␤1, plasminogen activator inhibitor-1, and several other extracellular matrix proteins compared with vehicle-treated SHR-SP.The renin-angiotensin system is a major regulator of blood pressure within the body, through the maintenance of vascular tone and sodium homeostasis. The renin-angiotensin system has, however, also been implicated in a number of diseases, characterized by remodeling and fibrosis, including forms of progressive renal disease. The generation of angiotensin II can lead to organ damage through both mitogenic activity and profibrotic remodeling. Eprosartan is a potent (K i ϭ 1.4 nM) angiotensin II receptor antagonist selective for the AT 1 subtype. AT 1 receptor antagonists have been shown to attenuate the effects of exogenous angiotensin II (Wang et al., 1997) and to be renoprotective in the partial nephrectomy model of renal failure (Gandhi et al., 1999), as measured by its ability to attenuate the hypertension, proteinuria, and up-regulation in the expression of several profibrotic genes associated with this model (Wong et al., 2000). TGF-␤ gene expression has been shown to be upregulated in a number of animal models of fibrotic disease, including renal disease (Border and Noble, 1998) and can be induced by several different vasoactive mitogens, including angiotensin II (Klahr and Morrissey, 2000). This profibrotic cytokine mediates the up-regulation of several extracellular matrix component genes, including fibronectin and collagen, leading to increased synthesis of the extracellular matrix (Ignotz and Massague, 1986). Furthermore, TGF...

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Section: Discussionsupporting

confidence: 92%

The Angiotensin Type 1 Receptor Antagonist, Eprosartan, Attenuates the Progression of Renal Disease in Spontaneously Hypertensive Stroke-Prone Rats with Accelerated Hypertension

Abrahamsen

Barone²,

Campbell³

et al. 2002

J Pharmacol Exp Ther

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“…Furthermore, the expression of TGF-β1 is a critical marker which can determine the progression of renal injury [25]. Our study revealed that all these indicators were attenuated by aliskiren treatment, suggesting that aliskiren has renoprotective effects in anti-GBM GN.…”

Section: Discussionmentioning

confidence: 65%

Aliskiren Regulates Neonatal Fc Receptor and IgG Metabolism with Attenuation of Anti-GBM Glomerulonephritis in Mice

Kang

Baik

Yoo

et al. 2016

Nephron

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Background: Renin, in addition to its activation of the renin-angiotensin system, binds to the (pro)renin receptor (PRR) and triggers inflammatory and fibrogenic signaling in tissue. In addition, aliskiren, a direct renin inhibitor, has been shown to affect IgG metabolism by altering PRR and neonatal Fc receptors (FcRns). Methods: We investigated the effect of aliskiren on proteinuria, glomerular extracellular matrix, expressions of fibronectin, transforming growth factor β1 (TGF-β1), PRR, FcRn and renal metabolism of IgG in a mice model of anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). Results: IgG deposition and expressions of FcRn and PRR were enhanced at glomeruli and urinary IgG levels increased in anti-GBM GN. Aliskiren attenuated anti-GBM GN with reduction of proteinuria and cortical expressions of fibronectin and TGF-β1. In addition, aliskiren suppressed the renal cortical expressions of FcRn and PRR. Aliskiren also reduced the glomerular IgG depositions and the urinary IgG levels albeit with increased circulating serum IgG levels. Conclusion: These results suggest that suppression of FcRn and PRR and regulation of IgG metabolism may be related to the attenuation of anti-GBM GN by aliskiren.

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“…Several lines of evidence have shown that Ang II contributes to the progression of renal injury in experimental glomerulonephritis (GN), as demonstrated by the alleviation of renal injury in GN associated with the inhibition of Ang II generation as well as the pharmacologic blockade or genetic disruption of AT1 (35)(36)(37). Taken together, these findings indicate that BNP inhibits the ERK phosphorylation induced by Ang II in the nephritic kidney, and consequently attenuates renal injury in GN.…”

Section: Fig 7 Mkp-1 and -2 Expression In The Ventricles Of Unstimumentioning

confidence: 90%

Angiotensin II-Induced Ventricular Hypertrophy and Extracellular Signal-Regulated Kinase Activation Are Suppressed in Mice Overexpressing Brain Natriuretic Peptide in Circulation

et al. 2003

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Role of Angiotensin II in the Transforming Growth Factor-.BETA.1 Expression of Rat Kidney in Anti-Glomerular Basement Membrane Antiserum-Induced Glomerulonephritis.

Cited by 14 publications

References 0 publications

The Angiotensin Type 1 Receptor Antagonist, Eprosartan, Attenuates the Progression of Renal Disease in Spontaneously Hypertensive Stroke-Prone Rats with Accelerated Hypertension

The Angiotensin Type 1 Receptor Antagonist, Eprosartan, Attenuates the Progression of Renal Disease in Spontaneously Hypertensive Stroke-Prone Rats with Accelerated Hypertension

Aliskiren Regulates Neonatal Fc Receptor and IgG Metabolism with Attenuation of Anti-GBM Glomerulonephritis in Mice

Angiotensin II-Induced Ventricular Hypertrophy and Extracellular Signal-Regulated Kinase Activation Are Suppressed in Mice Overexpressing Brain Natriuretic Peptide in Circulation

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