Determining lineage relationships in kidney development and disease
Author:
Publisher
Springer Science and Business Media LLC
Subject
Nephrology
Link
https://www.nature.com/articles/s41581-021-00485-5.pdf
Reference160 articles.
1. Kobayashi, A. et al. Six2 defines and regulates a multipotent self-renewing nephron progenitor population throughout mammalian kidney development. Cell Stem Cell 3, 169–181 (2008). This manuscript applied genetic lineage tracing in mice to identify a self-renewing progenitor population within the cap mesenchyme that gives rise to all segments of the epithelial nephron.
2. Taguchi, A. et al. Redefining the in vivo origin of metanephric nephron progenitors enables generation of complex kidney structures from pluripotent stem cells. Cell Stem Cell 14, 53–67 (2014). This study used lineage tracing to define the embryological orgins of the metanephric nephron progenitors, paving the way for future studies using human pluripotent stem cells to recreate these populations.
3. Barker, N. et al. Lgr5+ve stem/progenitor cells contribute to nephron formation during kidney development. Cell Rep. 2, 540–552 (2012). Lineage tracing for Lgr5-derived cells showed the presence of a clonal cellular expansion giving rise to the medial segment of the forming nephron in mouse.
4. Rinkevich, Y. et al. In vivo clonal analysis reveals lineage-restricted progenitor characteristics in mammalian kidney development, maintenance, and regeneration. Cell Rep. 7, 1270–1283 (2014). Using an adaptation of the Brainbow approach to unique fluorescent protein lineage tracing, this study investigated the origin of cells along the length of the developing, postnatal and repairing nephrons in mouse, concluding that there were tubular progenitors within individual nephron segments that contribute specifically to that segment during development and repair.
5. Lazzeri, E. et al. Endocycle-related tubular cell hypertrophy and progenitor proliferation recover renal function after acute kidney injury. Nat. Commun. 9, 1344 (2018). Using a combination of Confetti and FUCCI2 lineage tracing mouse models, this study discounted the proliferation of surviving tubular epithelial cells as the predominant reparative mechanism during acute kidney injury, instead demonstrating their hypertrophic response. Tubular repair was found to occur via a distinct subpopulation of Pax2 -expressing epithelial progenitors more resistant to apoptosis and possessing clonogenic capacity.
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