Proteinuric Potentials of Angiotensin II, (des-Asp1)-Angiotensin II, and (des-Asp1, des-Arg2)-Angiotensin II in Rats.

Terui, Jun; Tamoto, Koichi; Sudo, Jun-ichi

doi:10.1248/bpb.17.1516

Cited by 11 publications

(5 citation statements)

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“…18 AngIII causes proteinuria and increases growth-related, profibrotic and proinflammatory genes. 44,67,68 Increased renal AngII production and aminopeptidase A expression have been described in pathological settings associated to tissue RAS activation, such as hypertension, diabetes mellitus, nephritis, and AngII infusion. 69,70 These data indicate that although AngII is the main effector peptide of the renin angiotensin system other components of this system, such as AngIII, could play an active role in renal injury.…”

Section: Discussionmentioning

confidence: 99%

Systemic Infusion of Angiotensin II into Normal Rats Activates Nuclear Factor-κB and AP-1 in the Kidney

Ruíz-Ortega

Lorenzo

Rupérez

et al. 2001

The American Journal of Pathology

171

167

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Recent studies have pointed out the implication of angiotensin II (Ang II) in various pathological settings. However, the molecular mechanisms and the AngII receptor (AT) subtypes involved are not fully identified. We investigated whether AngII elicited the in vivo activation of nuclear transcription factors that play important roles in the pathogenesis of renal and vascular injury. Systemic infusion of Ang II into normal rats increased renal nuclear factor (NF)-kappaB and AP-1 binding activity that was associated with inflammatory cell infiltration and tubular damage. Interestingly, infiltrating cells presented activated NF-kappaB complexes, suggesting the involvement of AngII in inflammatory cell activation. When rats were treated with AT(1) or AT(2) receptor antagonists different responses were observed. The AT(1) antagonist diminished NF-kappaB activity in glomerular and tubular cells and abolished AP-1 in renal cells, improved tubular damage and normalized the arterial blood pressure. The AT(2) antagonist diminished mononuclear cell infiltration and NF-kappaB activity in glomerular and inflammatory cells, without any effect on AP-1 and blood pressure. These data suggest that AT(1) mainly mediates tubular injury via AP-1/NF-kappaB, whereas AT(2) receptor participates in the inflammatory cell infiltration in the kidney by NF-kappaB. Our results provide novel information on AngII receptor signaling and support the recent view of Ang II as a proinflammatory modulator.

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Section: Discussionmentioning

confidence: 99%

Systemic Infusion of Angiotensin II into Normal Rats Activates Nuclear Factor-κB and AP-1 in the Kidney

Ruíz-Ortega

Lorenzo

Rupérez

et al. 2001

The American Journal of Pathology

171

167

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“…AngIII is a chemoattractant for polymorphonuclear leukocytes and monocytes and regulates chemokine production (5,48). AngIII causes proteinuria and increases expression of growth-related and profibrotic genes (3,4). Inasmuch as elevated renal APA and AT 2 receptor expression and NF-B activity levels have been observed during kidney injury (6,11,12,46,47), AngIII, acting via the AT 2 receptor/NF-B pathway, could participate in the progression of renal damage.…”

Section: Discussionmentioning

confidence: 99%

“…Some actions originally attributed to AngII, such as vasopressin release, are attributable to AngIII (2). Recent data suggested that AngIII could be involved in renal pathophysiologic processes (3)(4)(5). In renal cells, AngIII increases angiotensinogen, transforming growth factor-␤, fibronectin, and monocyte chemoattractant protein-1 (MCP-1) gene expression (4,5); therefore, AngII could contribute to inflammation and fibrosis in the kidney.…”

mentioning

confidence: 99%

Angiotensin III Activates Nuclear Transcription Factor-κB in Cultured Mesangial Cells Mainly via AT2 Receptors

Lorenzo¹,

Ruíz-Ortega²,

Suzuki³

et al. 2002

Journal of the American Society of Nephrology

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ABSTRACT. Nuclear factor-κB (NF-κB) regulates many genes involved in renal pathophysiologic processes. It was previously demonstrated that angiotensin II (AngII) and its amino-terminal degradation product AngIII activate NF-κB in mesangial cells. However, which are the Ang receptor subtypes involved in the NF-κB pathway and whether these Ang peptides act through the same or different receptors in mesangial cells have not been evaluated. Under the culture conditions used, quiescent rat mesangial cells expressed both AT1and AT2receptors. To investigate the receptors involved in the NF-κB pathway, two different approaches were used,i.e., pharmacologic studies, using specific AT1and AT2receptor antagonists and agonists, and studies in AT1receptor-knockout mice. In cultured rat mesangial cells, both AT1and AT2receptor antagonists inhibited AngII-induced NF-κB DNA binding activity, whereas NF-κB activation elicited by AngIII was mainly blocked by the AT2receptor antagonist. Similar results were observed for cytosolic IκBα degradation. An AT2receptor agonist also activated NF-κB. In AT1receptor-knockout murine mesangial cells, AngIII and AngII increased NF-κB activity and degraded cytosolic IκBα; both processes were blocked by the AT2receptor antagonist. These data demonstrate that, in mesangial cells, NF-κB activation is mediated by AT1and AT2receptors, suggesting a novel intracellular signaling mechanism for AT2receptors in the kidney. Some differences in Ang peptide receptor-mediated responses were also observed. AngII activates NF-κB via AT1and AT2receptors, whereas AngIII acts mainly via AT2receptors. These results suggest the potential involvement of the AngIII/AT2receptor/NF-κB pathway in pathophysiologic processes in the kidney and provide a better understanding of the renin-angiotensin system.

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“…Many of the effects originally attributed to Ang II, such as vasopressin release, are found to be in response to Ang III (27). Other investigators suggested that Ang III might be involved in several renal pathophysiologic processes (28–30). Ang III has been demonstrated to increase kidney cell expression of angiotensinogen, transforming growth factor-β, fibronectin, and monocyte chemoattractant protein-1 (MCP-1) (29, 30).…”

mentioning

confidence: 99%

HIV-associated nephropathy: Role of AT2R

Salhan

Sagar

Kumar

et al. 2012

Cellular Signalling

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AT1R has been reported to play an important role in the progression of HIV-associated nephropathy (HIVAN); however, the effect of AT2R has not been studied. Age and sex matched control (FVB/N) and Tg26 mice aged 4, 8, and 16 weeks were studied for renal tissue expression of AT1R and AT2R (Protocol A). Renal tissue mRNA expression of AT2R was lower in Tg26 mice when compared with control mice. In protocol B, Tg26 mice were treated with either saline, telmisartan (TEL, AT1 blocker), PD123319 (PD, AT2R blocker), or TEL + PD for two weeks. TEL-receiving Tg26 (TRTg) displayed less advanced glomerular and tubular lesions when compared with saline-receiving Tg26 (SRTg). TRTgs displayed enhanced renal tissue AT2R expression when compared to SRTgs. Diminution of renal tissue AT2R expression was associated with advanced renal lesions in SRTgs; whereas, upregulation of AT2R expression in TRTgs was associated with attenuated renal lesions. PD-receiving Tg 26 mice (PDRTg) did not show any alteration in the course of HIVAN; whereas, PD + TEL-receiving Tg26 (PD-TRTg) showed worsening of renal lesions when compared to TRTgs. Interestingly, plasma as well as renal tissues of Tg26 mice displayed several fold higher concentration of Ang III, a ligand of AT2R.

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Proteinuric Potentials of Angiotensin II, (des-Asp1)-Angiotensin II, and (des-Asp1, des-Arg2)-Angiotensin II in Rats.

Cited by 11 publications

References 0 publications

Systemic Infusion of Angiotensin II into Normal Rats Activates Nuclear Factor-κB and AP-1 in the Kidney

Systemic Infusion of Angiotensin II into Normal Rats Activates Nuclear Factor-κB and AP-1 in the Kidney

Angiotensin III Activates Nuclear Transcription Factor-κB in Cultured Mesangial Cells Mainly via AT2 Receptors

HIV-associated nephropathy: Role of AT2R

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