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Flannery 2015 Abstract MiP2015 - Revision history
2024-03-29T15:44:06Z
Revision history for this page on the wiki
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https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=125305&oldid=prev
Beno Marija at 13:28, 9 November 2016
2016-11-09T13:28:55Z
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Beno Marija
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=97734&oldid=prev
Kandolf Georg at 14:07, 4 September 2015
2015-09-04T14:07:27Z
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=97725&oldid=prev
Kandolf Georg at 14:03, 4 September 2015
2015-09-04T14:03:54Z
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=96827&oldid=prev
Kandolf Georg at 06:31, 25 August 2015
2015-08-25T06:31:20Z
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MiP2015</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MiP2015</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|abstract=Mitochondrial dysfunction is a well-established hallmark of aging and neurodegenerative diseases. Maintenance of mitochondrial dynamics is essential for mitochondrial health maintenance and disturbances in mitochondrial dynamics have been implicated in a number of neurodegenerative processes. Moreover, patients with mutations in mitochondrial proteins involved in mitochondrial fusion, namely, Mfn2 and OPA1 genes have been associated with Charcot-Marie-Tooth disease type 2A, hereditary motor and sensory neuropathy VI, and autosomal optic atrophy (ADOA), respectively. In addition to its major role in mitochondrial fusion, OPA1 is an inner mitochondrial membrane protein which is involved in apoptosis, cristae structure, mtDNA replication maintenance and mitochondrial potential, all potential hallmarks of neurodegenerative conditions [1]. </div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|abstract=Mitochondrial dysfunction is a well-established hallmark of aging and neurodegenerative diseases. Maintenance of mitochondrial dynamics is essential for mitochondrial health maintenance and disturbances in mitochondrial dynamics have been implicated in a number of neurodegenerative processes. Moreover, patients with mutations in mitochondrial proteins involved in mitochondrial fusion, namely, <ins style="font-weight: bold; text-decoration: none;">''</ins>Mfn2<ins style="font-weight: bold; text-decoration: none;">'' </ins>and <ins style="font-weight: bold; text-decoration: none;">''</ins>OPA1<ins style="font-weight: bold; text-decoration: none;">'' </ins>genes have been associated with Charcot-Marie-Tooth disease type 2A, hereditary motor and sensory neuropathy VI, and autosomal optic atrophy (ADOA), respectively. In addition to its major role in mitochondrial fusion, <ins style="font-weight: bold; text-decoration: none;">''</ins>OPA1<ins style="font-weight: bold; text-decoration: none;">'' </ins>is an inner mitochondrial membrane protein which is involved in apoptosis, cristae structure, mtDNA replication maintenance and mitochondrial potential, all potential hallmarks of neurodegenerative conditions [1].</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>To study the role of mitochondrial fusion in neurodegenerative processes, we have adapted qualitative methods based on subjective classification of organelle morphology into defined categories to a quantitative protocol which uses mitotracker staining of the mitochondrial network followed by live-cell confocal imaging combined with Huygens Essential for deconvolution and image analysis. The output allows a quantitative assessment of mitochondrial length and volume in different physiological and disease conditions [2,3].</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>To study the role of mitochondrial fusion in neurodegenerative processes, we have adapted qualitative methods based on subjective classification of organelle morphology into defined categories to a quantitative protocol which uses mitotracker staining of the mitochondrial network followed by live-cell confocal imaging combined with Huygens Essential for deconvolution and image analysis. The output allows a quantitative assessment of mitochondrial length and volume in different physiological and disease conditions [2,3].</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Using this technique, we have successfully imaged the mitochondrial network with a high degree of cell-to- cell reproducibility in both control fibroblasts and patient-derived primary fibroblasts with carrying pathogenic OPA1 mutations. OPA1-mutant fibroblasts showed clear morphological changes when compared with control fibroblasts under both basal and mitochondrial OXPHOS stress conditions. </div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Using this technique, we have successfully imaged the mitochondrial network with a high degree of cell-to- cell reproducibility in both control fibroblasts and patient-derived primary fibroblasts with carrying pathogenic <ins style="font-weight: bold; text-decoration: none;">''</ins>OPA1<ins style="font-weight: bold; text-decoration: none;">'' </ins>mutations. <ins style="font-weight: bold; text-decoration: none;">''</ins>OPA1<ins style="font-weight: bold; text-decoration: none;">''</ins>-mutant fibroblasts showed clear morphological changes when compared with control fibroblasts under both basal and mitochondrial OXPHOS stress conditions.</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Our study demonstrates the advantages of in-depth quantitative analysis of mitochondrial network morphology by using a reproducible protocol that is applicable to a wide range of neurodegenerative diseases.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Our study demonstrates the advantages of in-depth quantitative analysis of mitochondrial network morphology by using a reproducible protocol that is applicable to a wide range of neurodegenerative diseases.</div></td></tr>
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=96825&oldid=prev
Kandolf Georg at 06:21, 25 August 2015
2015-08-25T06:21:35Z
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MiP2015</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MiP2015</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|abstract=Mitochondrial dysfunction is a well-established hallmark of aging and neurodegenerative diseases. Maintenance of mitochondrial dynamics is essential for mitochondrial health maintenance and disturbances in mitochondrial dynamics have been implicated in a number of neurodegenerative processes. Moreover, patients with mutations in mitochondrial proteins involved in mitochondrial fusion, namely, Mfn2 and OPA1 genes have been associated with Charcot-Marie-Tooth disease type 2A, hereditary motor and sensory neuropathy VI, and autosomal optic atrophy (ADOA), respectively. In addition to its major role in mitochondrial fusion, OPA1 is an inner mitochondrial membrane protein which is involved in apoptosis, cristae structure, mtDNA replication maintenance and mitochondrial potential, all potential hallmarks of neurodegenerative conditions [1]. </ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">To study the role of mitochondrial fusion in neurodegenerative processes, we have adapted qualitative methods based on subjective classification of organelle morphology into defined categories to a quantitative protocol which uses mitotracker staining of the mitochondrial network followed by live-cell confocal imaging combined with Huygens Essential for deconvolution and image analysis. The output allows a quantitative assessment of mitochondrial length and volume in different physiological and disease conditions [2,3].</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Using this technique, we have successfully imaged the mitochondrial network with a high degree of cell-to- cell reproducibility in both control fibroblasts and patient-derived primary fibroblasts with carrying pathogenic OPA1 mutations. OPA1-mutant fibroblasts showed clear morphological changes when compared with control fibroblasts under both basal and mitochondrial OXPHOS stress conditions. </ins></div></td></tr>
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<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|area=Instruments;methods, mt-Structure;fission;fusion, mt-Membrane, mtDNA;mt-genetics, mt-Medicine</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|model cell lines=Fibroblast</ins></div></td></tr>
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=96785&oldid=prev
Kandolf Georg at 15:01, 24 August 2015
2015-08-24T15:01:28Z
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 15:01, 24 August 2015</td>
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<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|title=Quantitative live-cell imaging of mitochondrial network morphology in neurodegenerative conditions.</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|authors=Flannery PJ, Sitarz K, Yu-Wai-Man P</ins></div></td></tr>
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<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|additional=MiP2015}}</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|additional=MiP2015</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> </div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Affiliations ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Affiliations ==</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Wellcome Trust Centre for Mitochondrial research, Institute of Genetic Research, Newcastle University; Newcastle upon Tyne, UK. - p.f.flannery@ncl.ac.uk</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">== References and acknowledgements ==</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">#Burte F, Carelli V, Chinnery PF (2015) Disturbed mitochondrial dynamics and neurodegenerative disorders. Nat Rev Neurol 11:11-24.</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">#Zanna C, Ghelli A, Karbowski M, Youle RJ, Schimpf S (2008) OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion. Brain 131:352-67.</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">#Kao Shu-Huei, Yen May-Yung, Wang An-Guor (2015) Changes in mitochondrial morphology and bioenergetics in human lymphoblastoid cells with four novel OPA1 mutations. Investigative Ophthalmology and Visual Science 56:4:2269-78.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">== References and acknowledgements ==</del></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Supported by the Medical Research Council (MRC, UK)</ins></div></td></tr>
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Kandolf Georg
https://wiki.oroboros.at/index.php?title=Flannery_2015_Abstract_MiP2015&diff=96778&oldid=prev
Kandolf Georg: Created page with "{{Abstract |year=2015 |event=MiP2015 }} {{Labeling |additional=MiP2015}} == Affiliations == == References and acknowledgements =="
2015-08-24T14:50:16Z
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Kandolf Georg