Origin of new cells in the adult kidney: results from genetic labeling techniques

被引:95
作者
Duffield, Jeremy S. [2 ]
Humphreys, Benjamin D. [1 ,2 ]
机构
[1] Brigham & Womens Hosp, Harvard Inst Med, Div Renal, Dept Med, Boston, MA 02115 USA
[2] Harvard Stem Cell Inst, Boston, MA USA
关键词
acute renal failure; renal fibrosis; renal stem cell; EPITHELIAL-MESENCHYMAL TRANSITION; BETA-CELLS; REPORTER MOUSE; LIVER FIBROSIS; STEM-CELLS; CRE; PROLIFERATION; LOCALIZATION; INTERSTITIUM; FIBROGENESIS;
D O I
10.1038/ki.2010.338
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
100201 [内科学]; 100221 [泌尿外科学];
摘要
For nearly 100 years, developmental biologists have utilized fate mapping to understand the contributions of progenitor populations to organogenesis. More recently, Cre-Lox technology has allowed genetic fate mapping in adult mice, clarifying cell hierarchies in adult kidney disease models. In ischemia-reperfusion injury, genetic labeling of epithelial cells has demonstrated that intrinsic epithelial cells are responsible for nephron repair and not an interstitial or other non-epithelial cell type. In fibrotic kidney injury, fate mapping techniques have strongly challenged the theory that epithelial cells traverse the basement membrane to become myofibroblasts in a process of epithelial-to-mesenchymal transition and also indicate that interstitial pericytes/perivascular fibroblasts are the authentic myofibroblast progenitor pool. This mini review will summarize the fate mapping approach in mice, convey recent developments in kidney disease models, and outline future opportunities to apply this technology to better understand the cellular mechanisms of adult kidney homeostasis and disease. Kidney International (2011) 79, 494-501; doi: 10.1038/ki.2010.338; published online 22 September 2010
引用
收藏
页码:494 / 501
页数:8
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