Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins

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 dur...

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Vydané v:	Proceedings of the National Academy of Sciences - PNAS Ročník 110; číslo 7; s. E593
Hlavní autori:	Zencak, Dusan, Schouwey, Karine, Chen, Danian, Ekström, Per, Tanger, Ellen, Bremner, Rod, van Lohuizen, Maarten, Arsenijevic, Yvan
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 12.02.2013
Predmet:	Analysis of Variance Animals Apoptosis - physiology Cell Cycle Proteins - metabolism E2F1 Transcription Factor - metabolism Epigenesis, Genetic - genetics Epigenesis, Genetic - physiology Gene Expression Regulation - genetics Gene Expression Regulation - physiology Histological Techniques Mice Mice, Knockout Microscopy, Fluorescence Polycomb Repressive Complex 1 - genetics Polycomb Repressive Complex 1 - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Retinal Degeneration - metabolism
ISSN:	1091-6490, 1091-6490
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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 Rd1 photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in Rd1 mice. Most importantly, genetic ablation of Bmi1 provided extensive photoreceptor survival and improvement of retinal function in Rd1 mice, mediated by a decrease in cell cycle markers and regulators independent of p16(Ink4a) and p19(Arf). 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.
AbstractList	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 Rd1 photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in Rd1 mice. Most importantly, genetic ablation of Bmi1 provided extensive photoreceptor survival and improvement of retinal function in Rd1 mice, mediated by a decrease in cell cycle markers and regulators independent of p16(Ink4a) and p19(Arf). 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.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 Rd1 photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in Rd1 mice. Most importantly, genetic ablation of Bmi1 provided extensive photoreceptor survival and improvement of retinal function in Rd1 mice, mediated by a decrease in cell cycle markers and regulators independent of p16(Ink4a) and p19(Arf). 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. 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 Rd1 photoreceptor death process. Deleting E2f1, a downstream target of CDKs, provided temporary protection in Rd1 mice. Most importantly, genetic ablation of Bmi1 provided extensive photoreceptor survival and improvement of retinal function in Rd1 mice, mediated by a decrease in cell cycle markers and regulators independent of p16(Ink4a) and p19(Arf). 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.
Author	Chen, Danian Ekström, Per van Lohuizen, Maarten Zencak, Dusan Schouwey, Karine Tanger, Ellen Arsenijevic, Yvan Bremner, Rod
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SubjectTerms	Analysis of Variance Animals Apoptosis - physiology Cell Cycle Proteins - metabolism E2F1 Transcription Factor - metabolism Epigenesis, Genetic - genetics Epigenesis, Genetic - physiology Gene Expression Regulation - genetics Gene Expression Regulation - physiology Histological Techniques Mice Mice, Knockout Microscopy, Fluorescence Polycomb Repressive Complex 1 - genetics Polycomb Repressive Complex 1 - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Retinal Degeneration - metabolism
Title	Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins
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