Blockade of the Kinin B1 Receptor Ameloriates Glomerulonephritis

Klein, Julie; Gonzalez, Julien; Decramer, Stéphane; Bandı́n, Isabel; Neau, Eric; Salant, David J.; Heeringa, Peter; Pesquero, J. B.; Schanstra, Joost P.; Bascands, Jean-Loup

doi:10.1681/asn.2009090887

Cited by 48 publications

(53 citation statements)

References 37 publications

(48 reference statements)

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“…Most published studies have focused on the phase of acute glomerular injury (which may be associated with impaired renal function in association with crescentic disease), while data on long-term follow-up to determine if the mice develop progressive tubulointerstitial fibrosis, tubular atrophy and renal insufficiency are sparse. Some studies have reported interstitial inflammation [59–61] and elevated serum creatinine levels but the latter are likely a consequence of severe glomerular damage [62, 63]. Our preliminary studies with NTS generated by the Shankland laboratory suggest that progressive tubulointerstitial disease requires repeated NTS injections [64].…”

Section: Alternative Mouse Ckd Modelsmentioning

confidence: 99%

Investigating mechanisms of chronic kidney disease in mouse models

et al. 2011

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Animal models of chronic kidney disease (CKD) are important experimental tools that are used to investigate novel mechanistic pathways and to validate potential new therapeutic interventions prior to pre-clinical testing in humans. Over the past several years, mouse CKD models have been extensively used for these purposes. Despite significant limitations, the model of unilateral ureteral obstruction (UUO) has essentially become the high throughput in vivo model, as it recapitulates the fundamental pathogenetic mechanisms that typify all forms of CKD in a relatively short time span. In addition, several alternative mouse models are available that can be used to validate new mechanistic paradigms and/or novel therapies. Several models are reviewed – both genetic and experimentally induced – that provide investigators with an opportunity to include renal functional study end-points together with quantitative measures of fibrosis severity, something that is not possible with the UUO model.

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Section: Alternative Mouse Ckd Modelsmentioning

confidence: 99%

Investigating mechanisms of chronic kidney disease in mouse models

et al. 2011

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“…Quantification was performed as described previously. 67 induced generation of PAI-1 and fibrin formation, key mediators of decreased kidney perfusion and oxygenation. 43 …”

Section: Effect Of Preconditioned Nanofibers On Lps-induced Rho Kinasmentioning

confidence: 99%

Peptide Nanofibers Preconditioned with Stem Cell Secretome Are Renoprotective

Wang

Bakota²,

Chang

et al. 2011

Journal of the American Society of Nephrology

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Stem cells may contribute to renal recovery following acute kidney injury, and this may occur through their secretion of cytokines, chemokines, and growth factors. Here, we developed an acellular, nanofiber-based preparation of self-assembled peptides to deliver the secretome of embryonic stem cells (ESCs). Using an integrated in vitro and in vivo approach, we found that nanofibers preconditioned with ESCs could reverse cell hyperpermeability and apoptosis in vitro and protect against lipopolysaccharideinduced acute kidney injury in vivo. The renoprotective effect of preconditioned nanofibers associated with an attenuation of Rho kinase activation. We also observed that the combined presence of follistatin, adiponectin, and secretory leukoprotease during preconditioning was essential to the renoprotective properties of the nanofibers. In summary, we developed a designer-peptide nanofiber that can serve as a delivery platform for the beneficial effects of stem cells without the problems of teratoma formation or limited cell engraftment and viability.

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“…While the mechanisms of acute NTS are more completely characterized than the later autologous phases, the acute NTS model of glomerular injury remains complex due to evidence of multiple targets in the glomerulus including decay accelerating factor [28], CD59 [29], and others [30]–[32]. Using mice backcrossed over 10× to C57BL/6, we injected PodΔ Myh9 (KO) mice versus DHet control and FF control littermates with sheep NTS (graciously provided by Dr. D. Salant) or with control sheep IgG.…”

Section: Resultsmentioning

confidence: 99%

Background Strain and the Differential Susceptibility of Podocyte-Specific Deletion of Myh9 on Murine Models of Experimental Glomerulosclerosis and HIV Nephropathy

et al. 2013

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We previously reported that podocyte-specific deletion of Myh9 (conventional myosin heavy chain 2A) in C57BL/6 mice does not cause spontaneous kidney disease but instead results in a predisposition to glomerulosclerosis in response to a second model of glomerular injury. In contrast, other investigators reported that podocyte-specific deletion of Myh9 (PodΔMyh9) resulted in spontaneous glomerulosclerosis in mice on a mixed background, suggesting that the glomerulosclerosis is dependent on background strain. In order to elucidate the cause of this strain dependent effect Podocin::Cre and Myh9flox alleles were backcrossed to mouse strain FVB/N, which is highly susceptible to glomerulosclerosis, with the aim of intercrossing susceptible FVB/N and resistant C57BL/6 mice in subsequent congenic analyses. However, after backcrossing mice to FVB/N and aging mice to 28 weeks, we found no evidence of glomerular disease in PodΔMyh9 mice vs control littermates (urine MAC ratio all p>0.05). We also tested C57BL/6 PodΔMyh9 mice for a predisposition to injury from models other than Adriamycin including HIV nephropathy (HIVAN), puromycin nephropathy, and sheep nephrotoxic serum. In the Tg26 model of HIVAN, we found that podocyte-specific deletion of Myh9 resulted in a modest hypersensitivity in adults compared to Tg26+ control littermates (urine MAC ratio, p<0.05 or less). In contrast, we found that PodΔMyh9 mice were not predisposed to injury in response to other injury models including puromycin nephropathy and sheep nephrotoxic serum. While the mechanism of injury in these models is not fully understood, we conclude that PodΔMyh9 results in a variable susceptibility to glomerulosclerosis in response to different models of glomerular injury. In addition, based on the lack of a spontaneous phenotype of glomerulosclerosis in both C57BL/6 and FVB/N mice, we propose that Myh9 is not absolutely required in adult podocytes.

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Blockade of the Kinin B1 Receptor Ameloriates Glomerulonephritis

Cited by 48 publications

References 37 publications

Investigating mechanisms of chronic kidney disease in mouse models

Investigating mechanisms of chronic kidney disease in mouse models

Peptide Nanofibers Preconditioned with Stem Cell Secretome Are Renoprotective

Background Strain and the Differential Susceptibility of Podocyte-Specific Deletion of Myh9 on Murine Models of Experimental Glomerulosclerosis and HIV Nephropathy

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