No aggravation of renal injury in apolipoprotein E knockout mice (ApoE-/-) after subtotal nephrectomy

Buzello, Moriz; Haas, Christian; Hauptmann, Frank; Gross, Marie Luise; Faulhaber, Jörg; Schultze‐Mosgau, Stefan; Ehmke, Heimo; Ritz, Eberhard; Amann, Kerstin

doi:10.1093/ndt/gfg578

Cited by 20 publications

(15 citation statements)

References 29 publications

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“…In agreement with previous studies on ApoE À/À mice, blood pressure did not increase after UNX [20,21] and the absence of left ventricular hypertrophy in the present study is also consistent with absence of hypertension. Of note, the SBP, heart weight, and the heart/body weight ratio were not altered by any treatment.…”

Section: Discussionsupporting

confidence: 94%

Oxidative stress after uninephrectomy alters heart morphology in the apolipoprotein E −/− mouse

Piecha

Koleganova

Gross

et al. 2008

Journal of Hypertension

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Section: Discussionsupporting

confidence: 94%

Oxidative stress after uninephrectomy alters heart morphology in the apolipoprotein E −/− mouse

Piecha

Koleganova

Gross

et al. 2008

Journal of Hypertension

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“…In the study by Wen et al (2002), Apoe À/À mice developed spontaneous glomerular lesions with macrophage accumulation, commonly with foam cell appearance, deposition of extracellular matrix, glomerular hyperplasia, and foci of mesangiolysis associated with capillary microaneurysms. On the other hand, in studies using uninephrectomy (UNX) and subtotal nephrectomy (SNX) on wild-type and Apoe À/À mice, Buzello et al (2004) did not observe a difference in renal or glomerular injury after reduction of renal mass.…”

mentioning

confidence: 90%

Quantitative Trait Loci for Urinary Albumin in Crosses Between C57BL/6J and A/J Inbred Mice in the Presence and Absence of Apoe

Doorenbos¹,

Tsaih

Sheehan

et al. 2008

Genetics

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We investigated the effect of apolipoprotein E (Apoe) on albuminuria in the males of two independent F 2 intercrosses between C57BL/6J and A/J mice, using wild-type inbred strains in the first cross and B6-Apoe À/À animals in the second cross. In the first cross, we identified three quantitative trait loci (QTL): chromosome (Chr) 2 [LOD 3.5, peak at 70 cM, confidence interval (C.I.) 28-88 cM]; Chr 9 (LOD 2.0, peak 5 cM, C.I. 5-25 cM); and Chr 19 (LOD 1.9, peak 49 cM, C.I. 23-54 cM). The Chr 2 and Chr 19 QTL were concordant with previously found QTL for renal damage in rat and human. The Chr 9 QTL was concordant with a locus found in rat. The second cross, testing only Apoe À/À progeny, did not identify any of these loci, but detected two other loci on Chr 4 (LOD 3.2, peak 54 cM, C.I. 29-73 cM) and Chr 6 (LOD 2.6, peak 33 cM, C.I. 11-61 cM), one of which was concordant with a QTL found in rat. The dependence of QTL detection on the presence of Apoe and the concordance of these QTL with rat and human kidney disease QTL suggest that Apoe plays a role in renal damage.

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“…Unilateral nephrectomy significantly increased atherosclerotic lesion size in Apolipoprotein E ( Apoe −/− ) mice, 8-11 where, different from wild-type (wt) mice, serum creatinine was significantly elevated after unilateral nephrectomy. 9, 11 Renal glomerular number was decreased in Apoe −/− compared to wt mice, but there was no evidence for accelerated progression of kidney disease.…”

Section: Introductionmentioning

confidence: 99%

Increased Atherosclerotic Lesion Formation and Vascular Leukocyte Accumulation in Renal Impairment Are Mediated by Interleukin-17A

Hertel

Koltsova

et al. 2013

Circulation Research

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Rationale Atherosclerosis is a major cause of death in patients with chronic kidney disease. Chronic inflammation of the arterial wall including invasion, proliferation and differentiation of leukocytes is important in atherosclerotic lesion development. How atherosclerotic inflammation is altered in renal impairment is incompletely understood. Objective This study analyzed leukocytes of the atherosclerotic aorta in mice with impaired and normal renal function and studied a mechanism for the alteration in aortic myeloid leukocytes. Methods and Results Unilateral nephrectomy significantly decreased glomerular filtration rate and increased atherosclerotic lesion size and aortic leukocyte numbers in two murine atherosclerosis models, Apolipoprotein E (Apoe−/−) and LDL receptor (LDLr−/−) deficient mice. The number of aortic myeloid cells increased significantly. They took up less oxidized LDL, while CD11c expression, interaction with T cells and aortic T cell proliferation were significantly enhanced in renal impairment. In human PBMC cultures, chronic kidney disease serum decreased lipid uptake and increased HLAII expression. Supplementation with Interleukin (IL)-17A similarly increased HLAII and CD11c expression and impaired oxLDL uptake. IL-17A expression was increased in atherosclerotic mice with renal impairment. Ablation of IL-17A in LDLr−/− mice by lethal irradiation and reconstitution with Il17a−/− bone marrow abolished the effect of renal impairment on aortic CD11b+ myeloid cell accumulation, CD11c expression and cell proliferation. Atherosclerotic lesion size was decreased to levels observed in normal kidney function. Conclusions Kidney function modifies arterial myeloid cell accumulation and phenotype in atherosclerosis. Our results suggest a central role for IL-17A in aggravation of vascular inflammation and atherosclerosis in renal impairment.

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No aggravation of renal injury in apolipoprotein E knockout mice (ApoE-/-) after subtotal nephrectomy

Cited by 20 publications

References 29 publications

Oxidative stress after uninephrectomy alters heart morphology in the apolipoprotein E −/− mouse

Oxidative stress after uninephrectomy alters heart morphology in the apolipoprotein E −/− mouse

Quantitative Trait Loci for Urinary Albumin in Crosses Between C57BL/6J and A/J Inbred Mice in the Presence and Absence of Apoe

Increased Atherosclerotic Lesion Formation and Vascular Leukocyte Accumulation in Renal Impairment Are Mediated by Interleukin-17A

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