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Meis1 regulates postnatal cardiomyocyte cell cycle arrest

Mahmoud, Ahmed I ; Kocabas, Fatih ; Muralidhar, Shalini A ; Kimura, Wataru ; Koura, Ahmed S ; Thet, Suwannee ; Porrello, Enzo R ; Sadek, Hesham A

Nature (London), 2013-05, Vol.497 (7448), p.249-253 [Periódico revisado por pares]

England: Nature Publishing Group

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Título:
Meis1 regulates postnatal cardiomyocyte cell cycle arrest
Autor: Mahmoud, Ahmed I ; Kocabas, Fatih ; Muralidhar, Shalini A ; Kimura, Wataru ; Koura, Ahmed S ; Thet, Suwannee ; Porrello, Enzo R ; Sadek, Hesham A
Assuntos: Alleles ; Animals ; Animals, Newborn ; Apoptosis ; Cardiomyocytes ; Cell cycle ; Cell Cycle Checkpoints ; Cell Proliferation ; Cellular control mechanisms ; Cyclin-Dependent Kinase Inhibitor p15 - metabolism ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Female ; Gene expression ; Heart ; Heart - anatomy & histology ; Heart - physiology ; Heart attacks ; Heart cells ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Kinases ; Male ; Mice ; Myeloid Ecotropic Viral Integration Site 1 Protein ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - metabolism ; Neoplasm Proteins - deficiency ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Proteins ; Regeneration ; Transcriptional Activation
É parte de: Nature (London), 2013-05, Vol.497 (7448), p.249-253
Descrição: The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal day 7 and the mechanisms of cardiomyocyte cell cycle arrest remain unclear. The homeodomain transcription factor Meis1 is required for normal cardiac development but its role in cardiomyocytes is unknown. Here we identify Meis1 as a critical regulator of the cardiomyocyte cell cycle. Meis1 deletion in mouse cardiomyocytes was sufficient for extension of the postnatal proliferative window of cardiomyocytes, and for re-activation of cardiomyocyte mitosis in the adult heart with no deleterious effect on cardiac function. In contrast, overexpression of Meis1 in cardiomyocytes decreased neonatal myocyte proliferation and inhibited neonatal heart regeneration. Finally, we show that Meis1 is required for transcriptional activation of the synergistic CDK inhibitors p15, p16 and p21. These results identify Meis1 as a critical transcriptional regulator of cardiomyocyte proliferation and a potential therapeutic target for heart regeneration.
Editor: England: Nature Publishing Group
Idioma: Inglês

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Meis1 regulates postnatal cardiomyocyte cell cycle arrest

Mahmoud, Ahmed I ; Kocabas, Fatih ; Muralidhar, Shalini A ; Kimura, Wataru ; Koura, Ahmed S ; Thet, Suwannee ; Porrello, Enzo R ; Sadek, Hesham A

England: Nature Publishing Group

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