Telomerase expression in the mammalian heart

  1. Lookup NU author(s)
  2. Dr Gavin Richardson
  3. Dr Suzanne Cormack
  4. Dr Andrew Owens
Author(s)Richardson GD, Breault D, Horrocks G, Cormack S, Hole H, Owens WA
Publication type Article
JournalFASEB Journal
Year2012
Volume26
Issue12
Pages4832-4840
ISSN (print)0892-6638
ISSN (electronic)1530-6860
Full text is available for this publication:
While the mammalian heart has low, but functionally significant, levels of telomerase expression, the cellular population responsible remains incompletely characterized. This study aimed to identify the cell types responsible for cardiac telomerase activity in neonatal, adult, and cryoinjured adult hearts using transgenic mice expressing green fluorescent protein (GFP), driven by the promoter for murine telomerase reverse transcriptase (mTert), which is a necessary and rate-limiting component of telomerase. A rare population of mTert-GFP-expressing cells was identified that possessed all detectable cardiac telomerase RNA and telomerase activity. It was heterogeneous and included cells coexpressing markers of cardiomyocytic, endothelial, and mesenchymal lineages, putative cardiac stem cell markers, and, interestingly, cardiomyocytes with a differentiated phenotype. Quantification using both flow cytometry and immunofluorescence identified a significant decline in mTert-GFP cells in adult animals compared to neonates (∼9- and ∼20-fold, respectively). Cardiac injury resulted in a ∼6.45-fold expansion of this population (P<0.005) compared with sham-operated controls. This study identifies the cells responsible for cardiac telomerase activity, demonstrates a significant diminution with age but a marked response to injury, and, given the relationship between telomerase activity and stem cell populations, suggests that they represent a potential target for further investigation of cardiac regenerative potential
PublisherFederation of American Societies for Experimental Biology
URLhttp://dx.doi.org/10.1096/fj.12-208843
DOI10.1096/fj.12-208843
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