Publication Date:
2014-05-09
Description:
If and how the heart regenerates after an injury event is highly debated. c-kit-expressing cardiac progenitor cells have been reported as the primary source for generation of new myocardium after injury. Here we generated two genetic approaches in mice to examine whether endogenous c-kit(+) cells contribute differentiated cardiomyocytes to the heart during development, with ageing or after injury in adulthood. A complementary DNA encoding either Cre recombinase or a tamoxifen-inducible MerCreMer chimaeric protein was targeted to the Kit locus in mice and then bred with reporter lines to permanently mark cell lineage. Endogenous c-kit(+) cells did produce new cardiomyocytes within the heart, although at a percentage of approximately 0.03 or less, and if a preponderance towards cellular fusion is considered, the percentage falls to below approximately 0.008. By contrast, c-kit(+) cells amply generated cardiac endothelial cells. Thus, endogenous c-kit(+) cells can generate cardiomyocytes within the heart, although probably at a functionally insignificant level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127035/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Berlo, Jop H -- Kanisicak, Onur -- Maillet, Marjorie -- Vagnozzi, Ronald J -- Karch, Jason -- Lin, Suh-Chin J -- Middleton, Ryan C -- Marban, Eduardo -- Molkentin, Jeffery D -- P01 HL108806/HL/NHLBI NIH HHS/ -- P50 HL052318/HL/NHLBI NIH HHS/ -- P50 HL077101/HL/NHLBI NIH HHS/ -- R00 HL112852/HL/NHLBI NIH HHS/ -- R01 HL105924/HL/NHLBI NIH HHS/ -- R37 HL060562/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 May 15;509(7500):337-41. doi: 10.1038/nature13309. Epub 2014 May 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA [2] Department of Medicine, division of Cardiology, Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota 55455, USA [3]. ; 1] Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA [2]. ; Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. ; Cedars-Sinai Heart Institute, 8700 Beverly Boulevard, Los Angeles, California 90048, USA. ; 1] Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA [2] Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24805242" target="_blank"〉PubMed〈/a〉
Keywords:
Aging/physiology
;
Animals
;
Cell Differentiation
;
Cell Fusion
;
*Cell Lineage
;
Endothelial Cells/cytology/metabolism
;
Female
;
Heart/growth & development
;
Heart Injuries/*pathology
;
Integrases/genetics/metabolism
;
Male
;
Mice
;
Models, Biological
;
Myoblasts, Cardiac/*cytology/*metabolism
;
Myocardium/*cytology
;
Myocytes, Cardiac/*cytology/metabolism
;
Proto-Oncogene Proteins c-kit/*metabolism
;
Regeneration/physiology
;
Tamoxifen/pharmacology
Print ISSN:
0028-0836
Electronic ISSN:
1476-4687
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
,
Natural Sciences in General
,
Physics
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