2018
DOI: 10.1016/j.kint.2018.01.014
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Detection of renin lineage cell transdifferentiation to podocytes in the kidney glomerulus with dual lineage tracing

Abstract: Understanding of cellular transdifferentiation is limited by the technical inability to track multiple lineages in vivo. To overcome this we developed a new tool to simultaneously fate map two distinct cell types in the kidney, and genetically test whether cells of renin lineage (CoRL) can transdifferentiate to a podocyte fate. Ren1cCreER/tdTomato/Nphs1-FLPo/FRT-EGFP mice (CoRL-PODO mice) were generated by crossing Ren1c-CreER/tdTomato CoRL reporter mice with Nphs1-FLPo/FRT-EGFP podocyte reporter mice. Followi… Show more

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Cited by 33 publications
(25 citation statements)
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“…The JGA is a specialized region of the nephron with critical roles in tubuloglomerular feedback and systemic blood pressure regulation. Recently, this region has gained increasing interest due to the putative role of renin-positive cells in mediating podocyte regeneration (28,29). The components of the JGA include the aforementioned renin-positive cells ( Figure 4H), as well as associated tubular segments that comprise the transition point from tALH to DCT ( Figure 4, I and J).…”
Section: Resultsmentioning
confidence: 99%
“…The JGA is a specialized region of the nephron with critical roles in tubuloglomerular feedback and systemic blood pressure regulation. Recently, this region has gained increasing interest due to the putative role of renin-positive cells in mediating podocyte regeneration (28,29). The components of the JGA include the aforementioned renin-positive cells ( Figure 4H), as well as associated tubular segments that comprise the transition point from tALH to DCT ( Figure 4, I and J).…”
Section: Resultsmentioning
confidence: 99%
“…PECs have also gained attention as potential sources of additional podocytes in the postnatal period (14). Recent publications have shown that podocyte regeneration may be possible in specific scenarios (45)(46)(47)(48)(49)(50)(51), but other publications have ruled this out (10,52). Conflicting evidence may highlight differences in glomerular injury models, mouse backgrounds, adequacy of wash-out periods, transgene leakiness, and quantification methods, among other factors.…”
Section: Discussionmentioning
confidence: 99%
“…Together, these observations support the intriguing possibility that PRSS23 is involved in the development of a migratory PEC-PC phenotype in glomerular disease. Other possible cells responsible for the signature gene expression include transdifferentiating renin lineage cells (41), which can migrate across the glomerular or mesangial basement membrane. However, our description of these 9 genes within the context of developing PCs provides more compelling evidence in support of PEC-PC phenotype plasticity.…”
Section: Discussionmentioning
confidence: 99%