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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</title>
<author><name sortKey="Zencak, Dusan" sort="Zencak, Dusan" uniqKey="Zencak D" first="Dusan" last="Zencak">Dusan Zencak</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Schouwey, Karine" sort="Schouwey, Karine" uniqKey="Schouwey K" first="Karine" last="Schouwey">Karine Schouwey</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Chen, Danian" sort="Chen, Danian" uniqKey="Chen D" first="Danian" last="Chen">Danian Chen</name>
<affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>
, Toronto, ON,<country>Canada</country>
M5T 2S8;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Ekstrom, Per" sort="Ekstrom, Per" uniqKey="Ekstrom P" first="Per" last="Ekström">Per Ekström</name>
<affiliation><nlm:aff wicri:cut="; and" id="aff3">Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>
, SE-221 84 Lund,<country>Sweden</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Tanger, Ellen" sort="Tanger, Ellen" uniqKey="Tanger E" first="Ellen" last="Tanger">Ellen Tanger</name>
<affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>
, 1066 CX, Amsterdam,<country>The Netherlands</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Bremner, Rod" sort="Bremner, Rod" uniqKey="Bremner R" first="Rod" last="Bremner">Rod Bremner</name>
<affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>
, Toronto, ON,<country>Canada</country>
M5T 2S8;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Van Lohuizen, Maarten" sort="Van Lohuizen, Maarten" uniqKey="Van Lohuizen M" first="Maarten" last="Van Lohuizen">Maarten Van Lohuizen</name>
<affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>
, 1066 CX, Amsterdam,<country>The Netherlands</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Arsenijevic, Yvan" sort="Arsenijevic, Yvan" uniqKey="Arsenijevic Y" first="Yvan" last="Arsenijevic">Yvan Arsenijevic</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">23359713</idno>
<idno type="pmc">3574927</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3574927</idno>
<idno type="RBID">PMC:3574927</idno>
<idno type="doi">10.1073/pnas.1108297110</idno>
<date when="2013">2013</date>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</title>
<author><name sortKey="Zencak, Dusan" sort="Zencak, Dusan" uniqKey="Zencak D" first="Dusan" last="Zencak">Dusan Zencak</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Schouwey, Karine" sort="Schouwey, Karine" uniqKey="Schouwey K" first="Karine" last="Schouwey">Karine Schouwey</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Chen, Danian" sort="Chen, Danian" uniqKey="Chen D" first="Danian" last="Chen">Danian Chen</name>
<affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>
, Toronto, ON,<country>Canada</country>
M5T 2S8;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Ekstrom, Per" sort="Ekstrom, Per" uniqKey="Ekstrom P" first="Per" last="Ekström">Per Ekström</name>
<affiliation><nlm:aff wicri:cut="; and" id="aff3">Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>
, SE-221 84 Lund,<country>Sweden</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Tanger, Ellen" sort="Tanger, Ellen" uniqKey="Tanger E" first="Ellen" last="Tanger">Ellen Tanger</name>
<affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>
, 1066 CX, Amsterdam,<country>The Netherlands</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Bremner, Rod" sort="Bremner, Rod" uniqKey="Bremner R" first="Rod" last="Bremner">Rod Bremner</name>
<affiliation><nlm:aff id="aff2">Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>
, Toronto, ON,<country>Canada</country>
M5T 2S8;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Van Lohuizen, Maarten" sort="Van Lohuizen, Maarten" uniqKey="Van Lohuizen M" first="Maarten" last="Van Lohuizen">Maarten Van Lohuizen</name>
<affiliation><nlm:aff id="aff4">Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>
, 1066 CX, Amsterdam,<country>The Netherlands</country>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Arsenijevic, Yvan" sort="Arsenijevic, Yvan" uniqKey="Arsenijevic Y" first="Yvan" last="Arsenijevic">Yvan Arsenijevic</name>
<affiliation><nlm:aff id="aff1">Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title>
<idno type="ISSN">0027-8424</idno>
<idno type="eISSN">1091-6490</idno>
<imprint><date when="2013">2013</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<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>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id>
<journal-id journal-id-type="iso-abbrev">Proc. Natl. Acad. Sci. U.S.A</journal-id>
<journal-id journal-id-type="hwp">pnas</journal-id>
<journal-id journal-id-type="pmc">pnas</journal-id>
<journal-id journal-id-type="publisher-id">PNAS</journal-id>
<journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title>
</journal-title-group>
<issn pub-type="ppub">0027-8424</issn>
<issn pub-type="epub">1091-6490</issn>
<publisher><publisher-name>National Academy of Sciences</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23359713</article-id>
<article-id pub-id-type="pmc">3574927</article-id>
<article-id pub-id-type="publisher-id">201108297</article-id>
<article-id pub-id-type="doi">10.1073/pnas.1108297110</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>PNAS Plus</subject>
</subj-group>
<subj-group subj-group-type="heading"><subject>Biological Sciences</subject>
<subj-group><subject>Neuroscience</subject>
</subj-group>
</subj-group>
<series-title>PNAS Plus</series-title>
</article-categories>
<title-group><article-title>Retinal degeneration depends on Bmi1 function and reactivation of cell cycle proteins</article-title>
<alt-title alt-title-type="short">Cell cycle proteins control retinal degeneration</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Zencak</surname>
<given-names>Dusan</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Schouwey</surname>
<given-names>Karine</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
<xref ref-type="author-notes" rid="fn1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Danian</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
<xref ref-type="author-notes" rid="fn1"><sup>1</sup>
</xref>
<xref ref-type="author-notes" rid="fn2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ekström</surname>
<given-names>Per</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tanger</surname>
<given-names>Ellen</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>d</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bremner</surname>
<given-names>Rod</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>van Lohuizen</surname>
<given-names>Maarten</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>d</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Arsenijevic</surname>
<given-names>Yvan</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>3</sup>
</xref>
</contrib>
<aff id="aff1"><sup>a</sup>
Unit of Gene Therapy and Stem Cell Biology, Jules-Gonin Eye Hospital,<institution>University of Lausanne</institution>
, 1004 Lausanne,<country>Switzerland</country>
;</aff>
<aff id="aff2"><sup>b</sup>
Toronto Western Research Institute, University Health Network, Samuel Lunenfeld Research Institute,<institution>University of Toronto</institution>
, Toronto, ON,<country>Canada</country>
M5T 2S8;</aff>
<aff id="aff3"><sup>c</sup>
Division of Ophthalmology, Department of Clinical Sciences,<institution>Lund University</institution>
, SE-221 84 Lund,<country>Sweden</country>
; and</aff>
<aff id="aff4"><sup>d</sup>
Division of Molecular Genetics<institution>and The Centre of Biomedical Genetics</institution>
, 1066 CX, Amsterdam,<country>The Netherlands</country>
</aff>
</contrib-group>
<author-notes><corresp id="cor1"><sup>3</sup>
To whom correspondence should be addressed. E-mail: <email>yvan.arsenijevic@fa2.ch</email>
.</corresp>
<fn fn-type="edited-by"><p>Edited by Ching-Hwa Sung, Weill Medical College of Cornell University, New York, NY, and accepted by the Editorial Board December 26, 2012 (received for review June 9, 2011)</p>
</fn>
<fn fn-type="con"><p>Author contributions: D.Z., K.S., D.C., P.E., R.B., M.v.L., and Y.A. designed research; D.Z., K.S., D.C., P.E., and E.T. performed research; M.v.L. contributed new reagents/analytic tools; D.Z., K.S., D.C., P.E., R.B., M.v.L., and Y.A. analyzed data; and D.Z., K.S., R.B., and Y.A. wrote the paper.</p>
</fn>
<fn fn-type="equal" id="fn1"><p><sup>1</sup>
K.S. and D.C. contributed equally to this work.</p>
</fn>
<fn fn-type="present-address" id="fn2"><p><sup>2</sup>
Present address: Department of Ophthalmology, Ophthalmic Laboratory of Molecular Medicine Research Center, and Torsten-Wiesel Research Institute of World Eye Organization, West China Hospital, Sichuan University, Chengdu 610041, China.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><day>12</day>
<month>2</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>28</day>
<month>1</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>28</day>
<month>1</month>
<year>2013</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>110</volume>
<issue>7</issue>
<fpage>E593</fpage>
<lpage>E601</lpage>
<page-range>E593–E601</page-range>
<permissions><license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:type="simple" xlink:href="pnas.201108297.pdf"></self-uri>
<self-uri content-type="author-summary-pdf" xlink:type="simple" xlink:href="pnas.201108297_summary.pdf"></self-uri>
<abstract id="d34e224"><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>
</abstract>
<kwd-group><kwd>blindness</kwd>
<kwd>neurodegeneration</kwd>
<kwd>polycomb</kwd>
</kwd-group>
<counts><page-count count="9"></page-count>
</counts>
<custom-meta-group><custom-meta><meta-name>author-summary</meta-name>
<meta-value><xref ref-type="other" rid="author-summary"></xref>
</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>
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