{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:48:18Z","timestamp":1787017698662,"version":"build-2736575974"},"reference-count":86,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,8,13]],"date-time":"2017-08-13T00:00:00Z","timestamp":1502582400000},"content-version":"vor","delay-in-days":224,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:p>\n                    Rett syndrome (RTT) is a neurodevelopmental disorder with mutations in the\n                    <jats:italic>MECP2<\/jats:italic>\n                    gene. Mostly girls are affected, and an apparently normal development is followed by cognitive impairment, motor dysfunction, epilepsy, and irregular breathing. Various indications suggest mitochondrial dysfunction. In Rett mice, brain ATP levels are reduced, mitochondria are leaking protons, and respiratory complexes are dysregulated. Furthermore, we found in MeCP2\u2010deficient mouse (\n                    <jats:italic>\n                      Mecp2\n                      <jats:sup>\u2212\/y<\/jats:sup>\n                    <\/jats:italic>\n                    ) hippocampus an intensified mitochondrial metabolism and ROS generation. We now used emission ratiometric 2\u2010photon imaging to assess mitochondrial morphology, mass, and membrane potential (\u0394\u03a8m) in\n                    <jats:italic>\n                      Mecp2\n                      <jats:sup>\u2212\/y<\/jats:sup>\n                    <\/jats:italic>\n                    hippocampal astrocytes. Cultured astrocytes were labeled with the \u0394\u03a8m marker JC\u20101, and semiautomated analyses yielded the number of mitochondria per cell, their morphology, and \u0394\u03a8m.\n                    <jats:italic>\n                      Mecp2\n                      <jats:sup>\u2212\/y<\/jats:sup>\n                    <\/jats:italic>\n                    astrocytes contained more mitochondria than wild\u2010type (WT) cells and were more oxidized. Mitochondrial size, \u0394\u03a8m, and vulnerability to pharmacological challenge did not differ. The antioxidant Trolox opposed the oxidative burden and decreased the mitochondrial mass, thereby dampening the differences among WT and\n                    <jats:italic>\n                      Mecp2\n                      <jats:sup>\u2212\/y<\/jats:sup>\n                    <\/jats:italic>\n                    astrocytes; mitochondrial size and \u0394\u03a8m were not markedly affected. In conclusion, mitochondrial alterations and redox imbalance in RTT also involve astrocytes. Mitochondria are more numerous in\n                    <jats:italic>\n                      Mecp2\n                      <jats:sup>\u2212\/y<\/jats:sup>\n                    <\/jats:italic>\n                    than in WT astrocytes. As this genotypic difference is abolished by Trolox, it seems linked to the oxidative stress in RTT.\n                  <\/jats:p>","DOI":"10.1155\/2017\/3064016","type":"journal-article","created":{"date-parts":[[2017,8,13]],"date-time":"2017-08-13T17:02:41Z","timestamp":1502643761000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Increased Mitochondrial Mass and Cytosolic Redox Imbalance in Hippocampal Astrocytes of a Mouse Model of Rett Syndrome: Subcellular Changes Revealed by Ratiometric Imaging of JC\u20101 and roGFP1 Fluorescence"],"prefix":"10.1155","volume":"2017","author":[{"given":"D\u00f6rthe F.","family":"Bebensee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8381-076X","authenticated-orcid":false,"given":"Karolina","family":"Can","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5863-1994","authenticated-orcid":false,"given":"Michael","family":"M\u00fcller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,8,13]]},"reference":[{"key":"e_1_2_8_1_2","first-page":"723","article-title":"\u00dcber ein eigenartiges hirnatrophisches Syndrom bei Hyperammon\u00e4mie im Kindesalter","volume":"116","author":"Rett A.","year":"1966","journal-title":"Wiener Medizinische Wochenschrift (1946)"},{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.410140412"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2007.10.001"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1985.tb10993.x"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1136\/jmg.2007.049452"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/13810"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/9780470515501.ch2"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1153252"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1086\/320109"},{"key":"e_1_2_8_10_2","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/9.16.2365"},{"key":"e_1_2_8_11_2","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.1320250506"},{"key":"e_1_2_8_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0387-7604(01)00331-X"},{"key":"e_1_2_8_13_2","first-page":"71","article-title":"Rett syndrome: analysis of deaths in the British survey","volume":"6","author":"Kerr A. 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