Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Wolf, Günter; Ziyadeh, Fuad N.; Thaiss, Friedrich; Tomaszewski, J; Caron, Rachel; Wenzel, Ulrich; Zahner, Gunther; Helmchen, Udo; Stahl, Rolf A.K.

doi:10.1172/jci119615

Cited by 232 publications

(198 citation statements)

References 53 publications

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“…The experiments with AT1 Ϫ/Ϫ MC revealed that those AngII actions were exerted mainly via AT1. These findings are consistent with previous studies showing that AngII, acting through both AT1 and AT2, induces T cell-chemokine production (12,33,52).…”

Section: Angii Enhances Th1-associated Chemokine Expression In MC Masupporting

confidence: 94%

Susceptibility to T Cell-Mediated Injury in Immune Complex Disease Is Linked to Local Activation of Renin-Angiotensin System: The Role of NF-AT Pathway

Suzuki

Gómez-Guerrero

Shirato³

et al. 2002

The Journal of Immunology

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FcR provides a critical link between ligands and effector cells in immune complex diseases. Emerging evidence reveals that angiotensin (Ang)II exerts a wide variety of cellular effects and contributes to the pathogenesis of inflammatory diseases. In anti-glomerular basement membrane Ab-induced glomerulonephritis (GN), we have previously noted that FcR-deficient mice (γ−/−) surviving from lethal initial damage still developed mesangial proliferative GN, which was drastically prevented by an AngII type 1 receptor (AT1) blocker. We further examined the mechanisms by which renin-Ang system (RAS) participates in this immune disease. Using bone marrow chimeras between γ−/− and AT1−/− mice, we found that glomerular injury in γ−/− mice was associated with CD4+ T cell infiltration depending on renal AT1-stimulation. Based on findings in cutaneous delayed-type hypersensitivity, we showed that AngII-activated renal resident cells are responsible for the recruitment of effector T cells. We next examined the chemotactic activity of AngII-stimulated mesangial cells, as potential mechanisms coupling RAS and cellular immunity. Chemotactic activity for T cells and Th1-associated chemokine (IFN-γ-inducible protein-10 and macrophage-inflammatory protein 1α) expression was markedly reduced in mesangial cells from AT1−/− mice. Moreover, this activity was mainly through calcineurin-dependent NF-AT. Although IFN-γ-inducible protein-10 was NF-κB-dependent, macrophage-inflammatory protein 1α was dominantly regulated by NF-AT. Furthermore, AT1-dependent NF-AT activation was observed in injured glomeruli by Southwestern histochemistry. In conclusion, our data indicate that local RAS activation, partly via the local NF-AT pathway, enhances the susceptibility to T cell-mediated injury in anti-glomerular basement membrane Ab-induced GN. This novel mechanism affords a rationale for the use of drugs interfering with RAS in immune renal diseases.

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Section: Angii Enhances Th1-associated Chemokine Expression In MC Masupporting

confidence: 94%

Susceptibility to T Cell-Mediated Injury in Immune Complex Disease Is Linked to Local Activation of Renin-Angiotensin System: The Role of NF-AT Pathway

Suzuki

Gómez-Guerrero

Shirato³

et al. 2002

The Journal of Immunology

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“…A transgenic study made by Arai directly demonstrated that overexpression of Ang II locally in rat glomeruli could lead to glomerulosclerosis (25). In addition to these studies, there have recently been reports of immunomodulatory effects of Ang II.For example, Wolf demonstrated that Ang II dose-dependently stimulated expression of RANTES, and modulated macrophages/monocytes recruitment in the kidneys (26).…”

Section: Discussionmentioning

confidence: 99%

Renal Protective Effects of Blocking the Intrarenal Renin-Angiotensin System.

Zhou

et al. 1999

Hypertens Res

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It has been well demonstrated that angiotensin-converting enzyme inhibitors (ACEIs) can retard the progression of renal failure and kidney sclerosis in patients and animal models with glomerular diseases. The aim of this study was to observe the influences of ACEI on intrarenal Ang II and TGFi81 local formation and their relation to renal protective effects. Experimental glomerulosclerosis with nephrotic syndrome was induced in unilateral nephrectomized rats with repeated injections of adriamycin. Rats were randomly divided into three groups: 1) a sham-operated control group (n = 8); 2) an NS group treated with ACE! (benazepril 4 mg/kg/d) (n =10), and 3) an NS group not treated (n =10). After 8 wk, serum, urine and renal tissue were collected for study. ACE activity and Ang II concentration in renal tissue were measured by colorimetry and radioimmunoassay, respectively. Immunohistochemistry staining was employed for transforming growth factor-,81 (TGF/91) and extracellular matrix (ECM) examination. .01 in all cases). In the ACEI treated group, these histologic benefits coincided with a reduced expression of TGFi91 in both tubular cells and sclerosed glomeruli in protein as well as mRNA level. These findings provide further evidence that ACE! (benazepril) can prevent the progression of renal damage in both the function and morphologic changes which associated with a down-regulation of intrarenal Ang II level through the relative inhibition of renal ACE activity. The blocking of the Intrarenal renin angiotensin system (RAS) might contribute to the inhibition of TGFj91 local formation and the TGFi91-mediated ECM accumulation that are related to the renal protective effects of ACE!. (Hypertens Res 1999; 22: 223-228)

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“…In general, AT 2 receptors represent about 14% of the Ang II receptor population in adult kidney with the remainder being AT 1 subtype (18). The distribution of renal AT 2 receptor subtypes has not been precisely determined with the exception of the apical receptor on proximal tubular epithelial cells and glomerular endothelial cells (1,19). Signaling linked to AT 2 receptor includes activation of MAPK phosphatase, NO, guanylate cyclase, and PLA 2 (1,20,21,22).…”

Section: Discussionmentioning

confidence: 99%

Arachidonic acid mediates angiotensin II effects on p21ras in renal proximal tubular cells via the tyrosine kinase-Shc-Grb2-Sos pathway

Jiao

Cui

Torti

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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In kidney epithelial cells, an angiotensin II (Ang II) type 2 receptor subtype (AT 2 ) is linked to a membrane-associated phospholipase A 2 (PLA 2 ) and the mitogenactivated protein kinase (MAPK) superfamily. However, the intervening steps in this linkage have not been determined. The aim of this study was to determine whether arachidonic acid mediates Ang II's effect on p21ras and if so, to ascertain the signaling mechanism(s). We observed that Ang II activated p21ras and that mepacrine, a phospholipase A 2 inhibitor, blocked this effect. This activation was also inhibited by PD123319, an AT 2 receptor antagonist but not by losartan, an AT 1 receptor antagonist. Furthermore, Ang II caused rapid tyrosine phosphorylation of Shc and its association with Grb2. Arachidonic acid and linoleic acid mimicked Ang II-induced tyrosine phosphorylation of Shc and activation of p21ras. Moreover, Ang II and arachidonic acid induced an association between p21ras and Shc. We demonstrate that arachidonic acid mediates linkage of a G protein-coupled receptor to p21ras via Shc tyrosine phosphorylation and association with Grb2͞Sos. These observations have important implications for other G protein-coupled receptors linked to a variety of phospholipases.

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Angiotensin II stimulates expression of the chemokine RANTES in rat glomerular endothelial cells. Role of the angiotensin type 2 receptor.

Cited by 232 publications

References 53 publications

Susceptibility to T Cell-Mediated Injury in Immune Complex Disease Is Linked to Local Activation of Renin-Angiotensin System: The Role of NF-AT Pathway

Susceptibility to T Cell-Mediated Injury in Immune Complex Disease Is Linked to Local Activation of Renin-Angiotensin System: The Role of NF-AT Pathway

Renal Protective Effects of Blocking the Intrarenal Renin-Angiotensin System.

Arachidonic acid mediates angiotensin II effects on p21ras in renal proximal tubular cells via the tyrosine kinase-Shc-Grb2-Sos pathway

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