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Cell Journal، جلد ۱۶، شماره Suppl ۱، صفحات ۱۲-۱۲
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عنوان انگلیسی Is-12: Kidney Regeneration - Glomerular Perspective
چکیده انگلیسی مقاله Objective: Podocyte loss is a major determinant of progressive chronic kidney disease. Although recent studies have shown that a subset of parietal epithelial cells can serve as podocyte progenitors, the role of podocyte regeneration in aging and nephron loss remains unclear. Materials and Methods: Here we combined genetic fate mapping with highly efficient podocyte isolation protocols to precisely quantify podocyte turnover. Results: We demonstrate for the first time that parietal epithelial cells can give rise to fully differentiated visceral epithelial cells indistinguishable from resident podocytes, and found that limited podocyte renewal occurs during glomerular development as well as in a diphtheria toxin-model of acute podocyte ablation. In contrast, the compensatory programs in response to nephron loss mainly evoke podocyte hypertrophy, but not podocyte regeneration. In addition, under physiological conditions no turnover of podocytes could be detected in aging mice. In the absence of podocyte replacement, progressive accumulation of oxidized proteins, deposits of protein aggregates, loss of podocytes and glomerulosclerosis were characteristic features of aging mouse kidneys. Conclusion: In summary, quantitative investigation of podocyte regeneration in vivo provides novel insights into the mechanism and capacity of podocyte regeneration in mice. Our data reveal that podocyte generation is mainly confined to glomerular development and occurs after acute glomerular injury, but fails to regenerate podocytes in aging kidneys or in response to nephron loss.
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/306
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