| Literature DB >> 22021716 |
Jie Song1, Suzanne Czerniak, Teresa Wang, Wendy Ying, Diana L Carlone, David T Breault, Benjamin D Humphreys.
Abstract
After acute kidney injury, mice with short telomeres develop increased damage with reduced proliferative capacity, which suggests an important role for telomere length in kidney repair. The enzyme telomerase reverse transcriptase (mTert) regulates telomere length; embryonic stem cells and certain adult stem cells express mTert, but whether cells in the adult kidney express mTert and whether these cells play a role in renal repair are unknown. Here, we found that telomerase protein and mRNA were highly enriched in renal papilla, a proposed niche of kidney stem cells. Using mTert-GFP reporter mice, we detected mTert in a subset of papillary epithelial cells comprising the collecting duct predominantly but also the loop of Henle. Approximately 5% of mTert-GFP(+) cells were label retaining, a characteristic of stem cells. mTert mRNA levels increased in renal papilla after ischemia-reperfusion injury, but genetically labeled mTert-expressing papillary cells neither divided nor migrated out of the renal papilla during kidney repair. In summary, these data suggest that cells expressing telomerase reverse transcriptase are not a progenitor-cell population, and they do not play a direct role in kidney repair.Entities:
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Year: 2011 PMID: 22021716 PMCID: PMC3250207 DOI: 10.1681/ASN.2011050447
Source DB: PubMed Journal: J Am Soc Nephrol ISSN: 1046-6673 Impact factor: 10.121