Parkinson's Disease in a Dish: What Patient Specific-Reprogrammed Somatic Cells Can Tell Us about Parkinson's Disease, If Anything?
Identifieur interne : 000C84 ( Pmc/Curation ); précédent : 000C83; suivant : 000C85Parkinson's Disease in a Dish: What Patient Specific-Reprogrammed Somatic Cells Can Tell Us about Parkinson's Disease, If Anything?
Auteurs : J. Drouin-Ouellet [Canada] ; R. A. Barker [Royaume-Uni]Source :
- Stem Cells International [ 1687-966X ] ; 2012.
Abstract
Technologies allowing for the derivation of patient-specific neurons from somatic cells are emerging as powerful
Url:
DOI: 10.1155/2012/926147
PubMed: 23316244
PubMed Central: 3539381
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkinson's Disease in a Dish: What Patient Specific-Reprogrammed Somatic Cells Can Tell Us about Parkinson's Disease, If Anything?</title><author><name sortKey="Drouin Ouellet, J" sort="Drouin Ouellet, J" uniqKey="Drouin Ouellet J" first="J." last="Drouin-Ouellet">J. Drouin-Ouellet</name><affiliation wicri:level="1"><nlm:aff id="I1">Neuroscience Axis, CHUL Research Center (CHUQ), T2-50, 2705 Boul. Laurier, Quebec City, QC, Canada G1V 4G2</nlm:aff><country>Canada</country><wicri:regionArea>Neuroscience Axis, CHUL Research Center (CHUQ), T2-50, 2705 Boul. Laurier, Quebec City, QC</wicri:regionArea></affiliation></author><author><name sortKey="Barker, R A" sort="Barker, R A" uniqKey="Barker R" first="R. A." last="Barker">R. A. Barker</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 0PY, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 0PY</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23316244</idno><idno type="pmc">3539381</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539381</idno><idno type="RBID">PMC:3539381</idno><idno type="doi">10.1155/2012/926147</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">000C84</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000C84</idno><idno type="wicri:Area/Pmc/Curation">000C84</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000C84</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Parkinson's Disease in a Dish: What Patient Specific-Reprogrammed Somatic Cells Can Tell Us about Parkinson's Disease, If Anything?</title><author><name sortKey="Drouin Ouellet, J" sort="Drouin Ouellet, J" uniqKey="Drouin Ouellet J" first="J." last="Drouin-Ouellet">J. Drouin-Ouellet</name><affiliation wicri:level="1"><nlm:aff id="I1">Neuroscience Axis, CHUL Research Center (CHUQ), T2-50, 2705 Boul. Laurier, Quebec City, QC, Canada G1V 4G2</nlm:aff><country>Canada</country><wicri:regionArea>Neuroscience Axis, CHUL Research Center (CHUQ), T2-50, 2705 Boul. Laurier, Quebec City, QC</wicri:regionArea></affiliation></author><author><name sortKey="Barker, R A" sort="Barker, R A" uniqKey="Barker R" first="R. A." last="Barker">R. A. Barker</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 0PY, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 0PY</wicri:regionArea></affiliation></author></analytic><series><title level="j">Stem Cells International</title><idno type="ISSN">1687-966X</idno><idno type="eISSN">1687-9678</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Technologies allowing for the derivation of patient-specific neurons from somatic cells are emerging as powerful <italic>in vitro</italic> tools to investigate the intrinsic cellular pathological behaviours of the diseases that affect these patients. While the use of patient-derived neurons to model Parkinson's disease (PD) has only just begun, these approaches have allowed us to begin investigating disease pathogenesis in a unique way. In this paper, we discuss the advances made in the field of cellular reprogramming to model PD and discuss the pros and cons associated with the use of such cells.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Chaudhuri, Kr" uniqKey="Chaudhuri K">KR Chaudhuri</name></author><author><name sortKey="Healy, Dg" uniqKey="Healy D">DG Healy</name></author><author><name sortKey="Schapira, Ahv" uniqKey="Schapira A">AHV Schapira</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lewis, Sjg" uniqKey="Lewis S">SJG Lewis</name></author><author><name sortKey="Barker, Ra" uniqKey="Barker R">RA Barker</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lowry, We" uniqKey="Lowry W">WE Lowry</name></author><author><name sortKey="Richter, L" uniqKey="Richter L">L Richter</name></author><author><name sortKey="Yachechko, R" uniqKey="Yachechko R">R 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Stem Cells Int</journal-id><journal-id journal-id-type="iso-abbrev">Stem Cells Int</journal-id><journal-id journal-id-type="publisher-id">SCI</journal-id><journal-title-group><journal-title>Stem Cells International</journal-title></journal-title-group><issn pub-type="ppub">1687-966X</issn><issn pub-type="epub">1687-9678</issn><publisher><publisher-name>Hindawi Publishing Corporation</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23316244</article-id><article-id pub-id-type="pmc">3539381</article-id><article-id pub-id-type="doi">10.1155/2012/926147</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title>Parkinson's Disease in a Dish: What Patient Specific-Reprogrammed Somatic Cells Can Tell Us about Parkinson's Disease, If Anything?</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Drouin-Ouellet</surname><given-names>J.</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Barker</surname><given-names>R. A.</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Neuroscience Axis, CHUL Research Center (CHUQ), T2-50, 2705 Boul. Laurier, Quebec City, QC, Canada G1V 4G2</aff><aff id="I2"><sup>2</sup>Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge, Cambridge CB2 0PY, UK</aff><author-notes><corresp id="cor1">*R. A. Barker: <email>rab46@cam.ac.uk</email></corresp><fn fn-type="other"><p>Academic Editor: Pavla Jendelova</p></fn></author-notes><pub-date pub-type="ppub"><year>2012</year></pub-date><pub-date pub-type="epub"><day>20</day><month>12</month><year>2012</year></pub-date><volume>2012</volume><elocation-id>926147</elocation-id><history><date date-type="received"><day>7</day><month>7</month><year>2012</year></date><date date-type="accepted"><day>3</day><month>12</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012 J. Drouin-Ouellet and R. A. Barker.</copyright-statement><copyright-year>2012</copyright-year><license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Technologies allowing for the derivation of patient-specific neurons from somatic cells are emerging as powerful <italic>in vitro</italic> tools to investigate the intrinsic cellular pathological behaviours of the diseases that affect these patients. While the use of patient-derived neurons to model Parkinson's disease (PD) has only just begun, these approaches have allowed us to begin investigating disease pathogenesis in a unique way. In this paper, we discuss the advances made in the field of cellular reprogramming to model PD and discuss the pros and cons associated with the use of such cells.</p></abstract></article-meta></front><floats-group><table-wrap id="tab1" orientation="portrait" position="float"><label>Table 1</label><caption><p>Summary of studies that have used dermal fibroblasts from PD patients to model the disease.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Forms of PD</th><th align="center" rowspan="1" colspan="1">Source of cells</th><th align="left" rowspan="1" colspan="1">Main findings</th><th align="center" rowspan="1" colspan="1">References</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">Sporadic</td><td align="center" rowspan="1" colspan="1"> </td><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1"> </td></tr><tr><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓</td><td align="left" rowspan="1" colspan="1">PD-specific iPS cells are able to generate dopaminergic neurons</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B21">11</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1">iPSC</td><td align="left" rowspan="1" colspan="1">New human iPS cell differentiation protocol to produce vmDA neuron</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B17">12</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1">↓<break></break>iDA</td><td align="left" rowspan="1" colspan="1">Morphological alterations (reduced numbers of neuritis and neurite arborization), accumulation of autophagic vacuoles</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B22">13</xref>]<break></break></td></tr><tr><td align="left" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓<break></break>iDA </td><td align="left" rowspan="1" colspan="1">Rapid and efficient induction of iDA from human PD patient fibroblasts</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B55">14</xref>]</td></tr><tr><td align="left" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="1" colspan="1">Familial</td><td align="center" rowspan="1" colspan="1"> </td><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1"> </td></tr><tr><td align="left" rowspan="1" colspan="1"> SNCA triplication</td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓</td><td align="left" rowspan="1" colspan="1">Accumulation of <italic>α</italic>-syn, inherent overexpression of markers of oxidative stress, and sensitivity to peroxide induced oxidative stress</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B28">15</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> SNCA triplication</td><td align="center" rowspan="1" colspan="1">iPSC</td><td align="left" rowspan="1" colspan="1">Production of double the amount of <italic>α</italic>-syn as neurons from the unaffected relative</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B27">16</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> SNCA A53T mutation</td><td align="center" rowspan="1" colspan="1">↓<break></break>iN/iDA</td><td align="left" rowspan="1" colspan="1">Successful genetic repair of the mutation</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B31">17</xref>]</td></tr><tr><td align="left" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="1" colspan="1"> LRRK2 G2019S <break></break> mutation</td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓</td><td align="left" rowspan="1" colspan="1">Increased expression of key oxidative stress-response genes and <italic>α</italic>-syn protein. Increased sensitivity to caspase-3 activation and cell death caused by exposure to stress agents</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B38">18</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> LRRK2 G2019S <break></break> mutation<break></break> </td><td align="center" rowspan="1" colspan="1">iPSC</td><td align="left" rowspan="1" colspan="1">Morphological alterations (reduced numbers of neurites and neurite arborization), accumulation of autophagic vacuoles</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B22">13</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> LRRK2 G2019S, <break></break> R1441C mutations</td><td align="center" rowspan="1" colspan="1">↓<break></break>iDA</td><td align="left" rowspan="1" colspan="1">Vulnerability associated with mitochondrial dysfunction which could be rescued with coenzyme Q10, rapamycin, and the LRRK2 inhibitor GW5074</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B39">19</xref>]</td></tr><tr><td align="left" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="1" colspan="1"> Parkin mutation</td><td align="center" rowspan="1" colspan="1"> </td><td align="left" rowspan="1" colspan="1">Increased transcription of monoamine oxidases and oxidative stress, reduced DA uptake and increased spontaneous DA release</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B48">20</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> PINK1 mutation</td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓<break></break><break></break>iPSC <break></break>iDA</td><td align="left" rowspan="1" colspan="1">Impaired recruitment to lentivirally expressed parkin to mitochondria, increased mitochondria copy number, upregulation of PGC-1<italic>α</italic>; corrected by lentiviral expression of wild-type PINK1</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B49">21</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1"> PINK1 Q456X <break></break> mutation</td><td align="center" rowspan="1" colspan="1"> </td><td align="left" rowspan="1" colspan="1">Vulnerability associated with mitochondrial dysfunction which could be rescued with coenzyme Q10, rapamycin, and the LRRK2 inhibitor GW5074</td><td align="center" rowspan="1" colspan="1">[<xref ref-type="bibr" rid="B39">19</xref>]</td></tr><tr><td align="left" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="1" colspan="1">Risk gene</td><td align="center" rowspan="1" colspan="1"> </td><td align="left" rowspan="1" colspan="1"> </td><td align="center" rowspan="1" colspan="1"> </td></tr><tr><td align="left" rowspan="1" colspan="1"> Glucocerebrosidase</td><td align="center" rowspan="1" colspan="1">Dermal fibroblasts <break></break>↓<break></break><break></break>iPSC <break></break><break></break>↓<break></break><break></break>iDA</td><td align="left" rowspan="1" colspan="1">Dramatic increase in <italic>α</italic>-syn protein levels with accumulation of <italic>α</italic>-syn, which results in neurotoxicity through aggregation dependent mechanisms</td><td align="center" rowspan="1" colspan="1"> [<xref ref-type="bibr" rid="B33">22</xref>]</td></tr></tbody></table><table-wrap-foot><fn><p>Abbreviations: <italic>α</italic>-syn: <italic>α</italic>-synuclein; DA: dopamine; iDA: induced dopaminergic neurons; iPS: induced pluripotent stem; LRRK2: Leucine-rich repeat kinase 2; PD: Parkinson's disease; PGC-1<italic>α</italic> Peroxisome proliferator-activated receptor-<italic>γ</italic> coactivator 1<italic>α</italic>; SNCA: <italic>α</italic>-synuclein gene; vmDA: ventral mesencephalon dopaminergic.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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