Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins
Identifieur interne : 000C80 ( Main/Exploration ); précédent : 000C79; suivant : 000C81Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins
Auteurs : Dusan Zencak [Suisse] ; Karine Schouwey [Suisse] ; Danian Chen [Canada] ; Per Ekström [Suède] ; Ellen Tanger [Pays-Bas] ; Rod Bremner [Canada] ; Maarten Van Lohuizen [Pays-Bas] ; Yvan Arsenijevic [Suisse]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2013.
Abstract
The epigenetic regulator Bmi1 controls proliferation in many organs. Reexpression of cell cycle proteins such as cyclin-dependent kinases (CDKs) is a hallmark of neuronal apoptosis in neurodegenerative diseases. Here we address the potential role of Bmi1 as a key regulator of cell cycle proteins during neuronal apoptosis. We show that several cell cycle proteins are expressed in different models of retinal degeneration and required in the
Url:
DOI: 10.1073/pnas.1108297110
PubMed: 23359713
PubMed Central: 3574927
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>The epigenetic regulator Bmi1 controls proliferation in many organs. Reexpression of cell cycle proteins such as cyclin-dependent kinases (CDKs) is a hallmark of neuronal apoptosis in neurodegenerative diseases. Here we address the potential role of Bmi1 as a key regulator of cell cycle proteins during neuronal apoptosis. We show that several cell cycle proteins are expressed in different models of retinal degeneration and required in the <italic>Rd1</italic>
photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in <italic>Rd1</italic>
mice. Most importantly, genetic ablation of <italic>Bmi1</italic>
provided extensive photoreceptor survival and improvement of retinal function in <italic>Rd1</italic>
mice, mediated by a decrease in cell cycle markers and regulators independent of p16<sup>Ink4a</sup>
and p19<sup>Arf</sup>
. These data reveal that Bmi1 controls the cell cycle-related death process, highlighting this pathway as a promising therapeutic target for neuroprotection in retinal dystrophies.</p>
</div>
</front>
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