{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:17:48Z","timestamp":1790201868620,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,6,11]],"date-time":"2016-06-11T00:00:00Z","timestamp":1465603200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004663","name":"Ministry of Science and Technology of Taiwan","doi-asserted-by":"crossref","award":["NSC-99-2320-B-006-019-MY3"],"award-info":[{"award-number":["NSC-99-2320-B-006-019-MY3"]}],"id":[{"id":"10.13039\/501100004663","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100004663","name":"Ministry of Science and Technology of Taiwan","doi-asserted-by":"crossref","award":["NSC-102-2320-B-006-012-MY3"],"award-info":[{"award-number":["NSC-102-2320-B-006-012-MY3"]}],"id":[{"id":"10.13039\/501100004663","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Pineal Research"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Mitochondrial dysfunction and oxidative stress are involved in the pathogenesis of\n                    <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>\n                    arkinson's disease (\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    ). Mitochondrial morphology is dynamic and precisely regulated by the mitochondrial fission and fusion machinery. Aberrant mitochondrial fragmentation controlled by the mitochondrial fission protein, dynamin\u2010related protein 1 (\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1), may result in cell death. Our previous results showed that melatonin protected neurons by inhibiting oxidative stress in a 1\u2010methyl\u20104\u2010phenylpyridinium (\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    )\u2010induced\n                    <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                    model. However, the effect of melatonin on mitochondrial dynamics remains uncharacterized. Herein, we investigated the effect of melatonin and the role of\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1 on\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    \u2010induced mitochondrial fission in rat primary cortical neurons. We found that\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    induced a rapid increase in the ratio of\n                    <jats:styled-content style=\"fixed-case\">GSSG<\/jats:styled-content>\n                    :total glutathione (a marker of oxidative stress) and mitochondrial fragmentation,\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1 upregulation within 4\u00a0hours, and finally resulted in neuron loss 48\u00a0hours after the treatment. Neurons overexpressing wild\u2010type\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1 promoted mitochondrial and nuclear fragmentation; however, neurons overexpressing dominant\u2010negative\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1\n                    <jats:sup>K38A<\/jats:sup>\n                    or cotreated with melatonin exhibited significantly reduced\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    \u2010induced mitochondrial fragmentation and neuron death. Moreover, melatonin cotreatment prevented an\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    \u2010induced high ratio of\n                    <jats:styled-content style=\"fixed-case\">GSSG<\/jats:styled-content>\n                    and mitochondrial\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1 upregulation. The prevention of mitochondrial fission by melatonin was not found in neurons transfected with wild\u2010type\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1. These results provide a new insight that the neuroprotective effect of melatonin against\n                    <jats:styled-content style=\"fixed-case\">MPP<\/jats:styled-content>\n                    <jats:sup>+<\/jats:sup>\n                    toxicity is mediated by inhibiting the oxidative stress and\n                    <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                    rp1\u2010mediated mitochondrial fragmentation.\n                  <\/jats:p>","DOI":"10.1111\/jpi.12343","type":"journal-article","created":{"date-parts":[[2016,5,9]],"date-time":"2016-05-09T14:57:10Z","timestamp":1462805830000},"page":"230-240","source":"Crossref","is-referenced-by-count":75,"title":["Melatonin prevents the dynamin\u2010related protein 1\u2010dependent mitochondrial fission and oxidative insult in the cortical neurons after 1\u2010methyl\u20104\u2010phenylpyridinium treatment"],"prefix":"10.1111","volume":"61","author":[{"given":"Jih\u2010Ing","family":"Chuang","sequence":"first","affiliation":[{"name":"Department of Physiology College of Medicine National Cheng Kung University  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I\u2010Ling","family":"Pan","sequence":"additional","affiliation":[{"name":"Department of Physiology College of Medicine National Cheng Kung University  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chia\u2010Yun","family":"Hsieh","sequence":"additional","affiliation":[{"name":"Department of Physiology College of Medicine National Cheng Kung University  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiu\u2010Ying","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Physiology College of Medicine National Cheng Kung University  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei\u2010Chun","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Physiology College of Medicine National Cheng Kung University  Tainan Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jyh Wei","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Parasitology College of Medicine National Cheng Kung University  Tainan 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