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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Attenuated Macrophage Infiltration in Glomeruli of Aged Mice Resulting in Ameliorated Kidney Injury in Nephrotoxic Serum Nephritis
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Attenuated Macrophage Infiltration in Glomeruli of Aged Mice Resulting in Ameliorated Kidney Injury in Nephrotoxic Serum Nephritis

机译:减毒在肾毒性血清肾炎中的肾小球肾小球中的巨噬细胞浸润导致肾脏损伤

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Senescent cells have deleterious effects on the tissue microenvironment through proinflammatory senescence-associated secretory phenotypes; meanwhile, the onset of glomerulonephritis is predominant in younger adults. To clarify the influence of aging on the onset and development of glomerulonephritis, we used a murine model of antibody-mediated nephritis. Sheep nephrotoxic serum was administered in C57BL/6J mice at 12 weeks (adult) or 18 months old (aged) after pre-immunization with sheep IgG. Depositions of sheep IgG and autologous mouse IgG along the glomerular basement membrane and the serum titer of anti-sheep IgG-specific mouse IgG were similar between adult and aged mice. However, kidney injury was depressed in aged mice, accompanied by reduced macrophage infiltration in the glomeruli. The mRNA expression of most chemokines involved in monocyte/macrophage chemotaxis was not different between adult and aged mice, but the cell surface expression of C-C chemokine receptor (CCR) 1 and CCR2 was down-regulated in the monocyte/macrophage lineage cells infiltrating the kidneys of aged nephritic mice. Furthermore, expression of all four isotypes of the Fc gamma receptor (Fc gamma R) was reduced in these cells. Both CCR and Fc gamma R expression were down-regulated in monocyte/macrophage lineage cells, resulting in attenuated glomerular infiltration of these cells and impaired glomerular injury in aged mice.
机译:衰老细胞通过促炎衰老相关的分泌表型对组织微环境有害影响;同时,肾小球肾炎的发病是较年轻的成年人的占主导地位。为了澄清老龄化对肾小球肾炎的发作和发展的影响,我们使用了抗体介导的肾炎的小鼠模型。在用绵羊IgG预防后,在12周(成人)或18个月(年龄)的12周(成人)或18个月(年龄)中施用绵羊肾毒性血清。沿着肾小球基底膜和抗羊IgG特异性小鼠IgG的绵羊IgG和自体小鼠IgG的沉积在成人和老年小鼠之间相似。然而,在老年小鼠中抑制了肾脏损伤,伴随着在肾小球中减少巨噬细胞浸润。参与单核细胞/巨噬细胞趋化性的大多数趋化因子的mRNA表达在成人和老年小鼠之间没有差异,但在渗透肾脏的单核细胞/巨噬细胞谱系细胞中,CC趋化因子受体(CCR)1和CCR2的细胞表面表达老年肾病小鼠。此外,在这些细胞中降低了Fcγ受体(Fcγr)的所有四个同样物的表达。 CCR和FCγR表达均在单核细胞/巨噬细胞谱系细胞中抑制,导致这些细胞的肾小球渗透和老年小鼠的肾小球损伤受损。

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