Adriamycin nephropathy in severe combined immunodeficient (SCID) mice

Lee, Vincent; Wang, Yiping; Qin, Xinghu; Wang, Ying; Zheng, Guoping; Mahajan, Deepika; Coombes, Jason D.; Rangan, Gopala K.; Alexander, Stephen; Harris, David C.H.

doi:10.1093/ndt/gfl413

Cited by 27 publications

(32 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…C57BL/c mice are highly resistant to adriamycin-induced renal injury, but renal injury may be inducible at higher doses (13-25 mg/ kg) than those required by BALB/c mice [21]. While most studies employ single injection regimen, regimens using multiple injections have also been reported [22][23][24][25]. After 16 weeks, the FSGS phenotype is observed with progression to global glomerulosclerosis and tubulointerstitial fibrosis at 24 weeks.…”

Section: Adriamycin Modelmentioning

confidence: 99%

Recent advances of animal model of focal segmental glomerulosclerosis

Yang

Dettmar

Kronbichler³

et al. 2018

Clin Exp Nephrol

View full text Add to dashboard Cite

In the last decade, great advances have been made in understanding the genetic basis for focal segmental glomerulosclerosis (FSGS). Animal models using specific gene disruption of the slit diaphragm and cytoskeleton of the foot process mirror the etiology of the human disease. Many animal models have been developed to understand the complex pathophysiology of FSGS. Therefore, we need to know the usefulness and exact methodology of creating animal models. Here, we review classic animal models and newly developed genetic animal models. Classic animal models of FSGS involve direct podocyte injury and indirect podocyte injury due to adaptive responses. However, the phenotype depends on the animal background. Renal ablation and direct podocyte toxin (PAN, adriamycin) models are leading animal models for FSGS, which have some limitations depending on mice background. A second group of animal models were developed using combinations of genetic mutation and toxin, such as NEP25, diphtheria toxin, and Thy1.1 models, which specifically injure podocytes. A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. More detailed information about podocytopathy and FSGS can be expected in the coming decade. Different animal models should be used to study FSGS depending on the specific aim and sometimes should be used in combination.

show abstract

Section: Adriamycin Modelmentioning

confidence: 99%

Recent advances of animal model of focal segmental glomerulosclerosis

Yang

Dettmar

Kronbichler³

et al. 2018

Clin Exp Nephrol

View full text Add to dashboard Cite

show abstract

“…In male Wistar rats, the dose of Adriamycin ranges between 1.5 and 7.5 mg/kg. Male BALB/c mice require 9.8–10.4 mg/kg, 9 while male BALB/c SCID mice, an inbred lymphocyte‐depleted strain of BALB/c mice, require only 5.3 mg/kg 10 . C57BL/c mice are highly resistant to Adriamycin‐induced renal injury but renal injury may be inducible at higher doses (13–25 mg/kg) 11–13 than those required in BALB/c mice.…”

Section: Administrationmentioning

confidence: 99%

“…Lymphocyte number is a determinant of sensitivity to Adriamycin‐induced renal injury. Compared with wild‐type BALB/c mice, SCID BALB/c require only half the dose of Adriamycin to induce disease 10 However, Adriamycin does not cause renal injury in lymphocyte‐depleted recombinase activating gene‐1 knockout C57BL/6 mice (V. Lee, unpubl. obs., 2010) meaning that lymphocyte number alone does not explain the resistance of C57BL/6 mice to Adriamycin‐induced renal injury.…”

Section: Genetic Susceptibilitymentioning

confidence: 99%

Adriamycin nephropathy: A model of focal segmental glomerulosclerosis

2010

View full text Add to dashboard Cite

This review provides a comprehensive overview of experimental adriamycin nephropathy, including analysis of its strengths and weaknesses, pathogenic mechanisms and practical advice on how best to perform this animal model of chronic kidney disease. ABSTRACT:Adriamycin nephropathy (AN) is a rodent model of chronic kidney disease that has been studied extensively and has enabled a greater understanding of the processes underlying the progression of chronic proteinuric renal disease. AN is characterized by podocyte injury followed by glomerulosclerosis, tubulointerstitial inflammation and fibrosis. Genetic studies have demonstrated a number of loci that alter both risk and severity of renal injury induced by Adriamycin. Adriamycin-induced renal injury has been shown in numerous studies to be modulated by both non-immune and immune factors, and has facilitated further study of mechanisms of tubulointerstitial injury. This review will outline the pharmacological behaviour of Adriamycin, and describe in detail the model of AN, including its key structural characteristics, genetic susceptibility and pathogenesis.

show abstract

“…Glomerulosclerosis, tubular atrophy, interstitial volume, and interstitial fibrosis were evaluated using methods described previously. 33 Briefly, images viewed under a light microscope were digitalized using a video camera and then transferred onto computer screen (Tang Computer, Sydney, Australia) using image analysis software (Optimas 5; Media Cybernetics, Seattle, WA). The outline of the glomerular capillary tuft was traced, and the computed area was used as a measure of total glomerular area.…”

Section: Histology and Immunohistochemistrymentioning

confidence: 99%

IL-10/TGF-β–Modified Macrophages Induce Regulatory T Cells and Protect against Adriamycin Nephrosis

Cao

Wang²,

Zheng³

et al. 2010

Journal of the American Society of Nephrology

242

210

View full text Add to dashboard Cite

IL-10/TGF-␤-modified macrophages, a subset of activated macrophages, produce anti-inflammatory cytokines, suggesting that they may protect against inflammation-mediated injury. Here, macrophages modified ex vivo by IL-10/TGF-␤ (IL-10/TGF-␤ ⌴2) significantly attenuated renal inflammation, structural injury, and functional decline in murine adriamycin nephrosis (AN). These cells deactivated effector macrophages and inhibited CD4 ϩ T cell proliferation. IL-10/TGF-␤ ⌴2 expressed high levels of the regulatory co-stimulatory molecule B7-H4, induced regulatory T cells from CD4 cells in vitro,and increased the number of regulatory T cells in lymph nodes draining the kidneys in AN. The phenotype of IL-10/TGF-␤ ⌴2 did not switch to that of effector macrophages in the inflamed kidney, and these cells did not promote fibrosis. Taken together, these data demonstrate that IL-10/TGF-␤-modified macrophages effectively protect against renal injury in AN and may become part of a therapeutic strategy for chronic inflammatory disease.

show abstract

Adriamycin nephropathy in severe combined immunodeficient (SCID) mice

Cited by 27 publications

References 8 publications

Recent advances of animal model of focal segmental glomerulosclerosis

Recent advances of animal model of focal segmental glomerulosclerosis

Adriamycin nephropathy: A model of focal segmental glomerulosclerosis

IL-10/TGF-β–Modified Macrophages Induce Regulatory T Cells and Protect against Adriamycin Nephrosis

Contact Info

Product

Resources

About