Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss
Abstract During normal aging, the number of dopaminergic (DA) neurons in the substantia nigra (SN) progressively diminishes, while massive DA neuronal loss is a hallmark sign of Parkinson’s disease (PD). Unfortunately, there is little known about the molecular events involved in age-related DA neuro...
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| Veröffentlicht in: | Neurobiology of aging 2016-05, Vol.41, p.1-10 |
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| creator | Lee, Yun-Il Kang, Hojin Ha, Young Wan Chang, Ki-Young Cho, Sung-Chun Song, Sang Ok Kim, Hyein Jo, Areum Khang, Rin Choi, Jeong-Yun Lee, Yunjong Park, Sang Chul Shin, Joo-Ho |
| description | Abstract During normal aging, the number of dopaminergic (DA) neurons in the substantia nigra (SN) progressively diminishes, while massive DA neuronal loss is a hallmark sign of Parkinson’s disease (PD). Unfortunately, there is little known about the molecular events involved in age-related DA neuronal loss. In this study, we found that (1) the level of parkin was decreased in the cerebellum, brain stem, SN, and striatum of aged mice, (2) diaminodiphenyl sulfone (DDS) restored the level of parkin, (3) DDS prevented age-dependent DA neuronal loss, and (4) DDS protected SH-SY5Y cells from MPP+ and H2 O2 . Furthermore, pre/post-treatment of DDS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model attenuated DA neuronal loss and restored motor behavior. DDS transcriptionally activated parkin via PERK-ATF4 signaling and DDS not only failed to induce parkin expression, but also failed to rescue SH-SY5Y cells from MPP+ in the absence of ATF4. Herein, we demonstrated for the first time that DDS increased parkin level and served as a neuroprotective agent for age-dependent DA neuronal loss. Thus, DDS may be a potential therapeutic agent for age-related neurodegeneration. |
| doi_str_mv | 10.1016/j.neurobiolaging.2015.11.008 |
| format | Article |
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Unfortunately, there is little known about the molecular events involved in age-related DA neuronal loss. In this study, we found that (1) the level of parkin was decreased in the cerebellum, brain stem, SN, and striatum of aged mice, (2) diaminodiphenyl sulfone (DDS) restored the level of parkin, (3) DDS prevented age-dependent DA neuronal loss, and (4) DDS protected SH-SY5Y cells from MPP+ and H2 O2 . Furthermore, pre/post-treatment of DDS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model attenuated DA neuronal loss and restored motor behavior. DDS transcriptionally activated parkin via PERK-ATF4 signaling and DDS not only failed to induce parkin expression, but also failed to rescue SH-SY5Y cells from MPP+ in the absence of ATF4. Herein, we demonstrated for the first time that DDS increased parkin level and served as a neuroprotective agent for age-dependent DA neuronal loss. Thus, DDS may be a potential therapeutic agent for age-related neurodegeneration.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2015.11.008</identifier><identifier>PMID: 27103513</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Activating Transcription Factor 4 - physiology ; Aging ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Brain - metabolism ; Cells, Cultured ; Dapsone - pharmacology ; Dapsone - therapeutic use ; Diaminodiphenyl sulfone ; Disease Models, Animal ; Dopaminergic neuron ; Dopaminergic Neurons - pathology ; eIF-2 Kinase - physiology ; Endoplasmic Reticulum Stress ; ER stress ; Female ; Internal Medicine ; Male ; Mice, Inbred C57BL ; Neurology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Parkin ; Parkinson Disease - drug therapy ; Parkinson Disease - pathology ; Parkinson's disease ; PERK-ATF4 signaling ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Substantia Nigra - cytology ; Substantia Nigra - pathology ; Ubiquitin-Protein Ligases - deficiency ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Neurobiology of aging, 2016-05, Vol.41, p.1-10</ispartof><rights>Elsevier Inc.</rights><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-7e368ae9ae2e86e7525a9b8933111f673b6b888230b81cbe8828f953be1caa9f3</citedby><cites>FETCH-LOGICAL-c474t-7e368ae9ae2e86e7525a9b8933111f673b6b888230b81cbe8828f953be1caa9f3</cites><orcidid>0000-0002-0425-3377 ; 0000-0002-0499-4589</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neurobiolaging.2015.11.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27103513$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Yun-Il</creatorcontrib><creatorcontrib>Kang, Hojin</creatorcontrib><creatorcontrib>Ha, Young Wan</creatorcontrib><creatorcontrib>Chang, Ki-Young</creatorcontrib><creatorcontrib>Cho, Sung-Chun</creatorcontrib><creatorcontrib>Song, Sang Ok</creatorcontrib><creatorcontrib>Kim, Hyein</creatorcontrib><creatorcontrib>Jo, Areum</creatorcontrib><creatorcontrib>Khang, Rin</creatorcontrib><creatorcontrib>Choi, Jeong-Yun</creatorcontrib><creatorcontrib>Lee, Yunjong</creatorcontrib><creatorcontrib>Park, Sang Chul</creatorcontrib><creatorcontrib>Shin, Joo-Ho</creatorcontrib><title>Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract During normal aging, the number of dopaminergic (DA) neurons in the substantia nigra (SN) progressively diminishes, while massive DA neuronal loss is a hallmark sign of Parkinson’s disease (PD). Unfortunately, there is little known about the molecular events involved in age-related DA neuronal loss. In this study, we found that (1) the level of parkin was decreased in the cerebellum, brain stem, SN, and striatum of aged mice, (2) diaminodiphenyl sulfone (DDS) restored the level of parkin, (3) DDS prevented age-dependent DA neuronal loss, and (4) DDS protected SH-SY5Y cells from MPP+ and H2 O2 . Furthermore, pre/post-treatment of DDS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model attenuated DA neuronal loss and restored motor behavior. DDS transcriptionally activated parkin via PERK-ATF4 signaling and DDS not only failed to induce parkin expression, but also failed to rescue SH-SY5Y cells from MPP+ in the absence of ATF4. Herein, we demonstrated for the first time that DDS increased parkin level and served as a neuroprotective agent for age-dependent DA neuronal loss. Thus, DDS may be a potential therapeutic agent for age-related neurodegeneration.</description><subject>Activating Transcription Factor 4 - physiology</subject><subject>Aging</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Brain - metabolism</subject><subject>Cells, Cultured</subject><subject>Dapsone - pharmacology</subject><subject>Dapsone - therapeutic use</subject><subject>Diaminodiphenyl sulfone</subject><subject>Disease Models, Animal</subject><subject>Dopaminergic neuron</subject><subject>Dopaminergic Neurons - pathology</subject><subject>eIF-2 Kinase - physiology</subject><subject>Endoplasmic Reticulum Stress</subject><subject>ER stress</subject><subject>Female</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Neurology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Parkin</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson's disease</subject><subject>PERK-ATF4 signaling</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Substantia Nigra - cytology</subject><subject>Substantia Nigra - pathology</subject><subject>Ubiquitin-Protein Ligases - deficiency</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkFv1DAQhS0EokvhL6AcOHBJ8MRx7EgICRXaIlXiAJw4WI4zWbx17GAnlfbf47AFCS5w8hzefON5bwh5AbQCCu2rQ-VxjaG3wem99fuqpsArgIpS-YDsgHNZQtOJh2RHoRNlwyU9I09SOlBKRSPax-SsFkAZB7YjX99ZPVkfBjt_Q390RVrdGDyW1g-rwaGYdby1vtATOhuiXjAVeo_lgDP6Af1SDGHeCBj31hQ_v-a1K1xI6Sl5NGqX8Nn9e06-XL7_fHFd3ny8-nDx9qY0jWiWUiBrpcZOY42yRcFrrrtedowBwNgK1re9lLJmtJdgesylHDvOegSjdTeyc_LyxJ1j-L5iWtRkk0HntMewJgWio5lGM-LfUsm6GngLWfr6JDUx7xJxVHO0k45HBVRtSaiD-jMJtSWhAFROIrc_v5-09hMOv5t_WZ8FlycBZmvuLEaVjEWfPbcRzaKGYP930pu_QMZZb412t3jEdAhrzInk3VSqFVWftqvYjgI4pbylLfsBdfC48w</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Lee, Yun-Il</creator><creator>Kang, Hojin</creator><creator>Ha, Young Wan</creator><creator>Chang, Ki-Young</creator><creator>Cho, Sung-Chun</creator><creator>Song, Sang Ok</creator><creator>Kim, Hyein</creator><creator>Jo, Areum</creator><creator>Khang, Rin</creator><creator>Choi, Jeong-Yun</creator><creator>Lee, Yunjong</creator><creator>Park, Sang Chul</creator><creator>Shin, Joo-Ho</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope><orcidid>https://orcid.org/0000-0002-0425-3377</orcidid><orcidid>https://orcid.org/0000-0002-0499-4589</orcidid></search><sort><creationdate>20160501</creationdate><title>Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss</title><author>Lee, Yun-Il ; Kang, Hojin ; Ha, Young Wan ; Chang, Ki-Young ; Cho, Sung-Chun ; Song, Sang Ok ; Kim, Hyein ; Jo, Areum ; Khang, Rin ; Choi, Jeong-Yun ; Lee, Yunjong ; Park, Sang Chul ; Shin, Joo-Ho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-7e368ae9ae2e86e7525a9b8933111f673b6b888230b81cbe8828f953be1caa9f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Activating Transcription Factor 4 - physiology</topic><topic>Aging</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Brain - metabolism</topic><topic>Cells, Cultured</topic><topic>Dapsone - pharmacology</topic><topic>Dapsone - therapeutic use</topic><topic>Diaminodiphenyl sulfone</topic><topic>Disease Models, Animal</topic><topic>Dopaminergic neuron</topic><topic>Dopaminergic Neurons - pathology</topic><topic>eIF-2 Kinase - physiology</topic><topic>Endoplasmic Reticulum Stress</topic><topic>ER stress</topic><topic>Female</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Neurology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Parkin</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson's disease</topic><topic>PERK-ATF4 signaling</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Substantia Nigra - cytology</topic><topic>Substantia Nigra - pathology</topic><topic>Ubiquitin-Protein Ligases - deficiency</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Yun-Il</creatorcontrib><creatorcontrib>Kang, Hojin</creatorcontrib><creatorcontrib>Ha, Young Wan</creatorcontrib><creatorcontrib>Chang, Ki-Young</creatorcontrib><creatorcontrib>Cho, Sung-Chun</creatorcontrib><creatorcontrib>Song, Sang Ok</creatorcontrib><creatorcontrib>Kim, Hyein</creatorcontrib><creatorcontrib>Jo, Areum</creatorcontrib><creatorcontrib>Khang, Rin</creatorcontrib><creatorcontrib>Choi, Jeong-Yun</creatorcontrib><creatorcontrib>Lee, Yunjong</creatorcontrib><creatorcontrib>Park, Sang Chul</creatorcontrib><creatorcontrib>Shin, Joo-Ho</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Yun-Il</au><au>Kang, Hojin</au><au>Ha, Young Wan</au><au>Chang, Ki-Young</au><au>Cho, Sung-Chun</au><au>Song, Sang Ok</au><au>Kim, Hyein</au><au>Jo, Areum</au><au>Khang, Rin</au><au>Choi, Jeong-Yun</au><au>Lee, Yunjong</au><au>Park, Sang Chul</au><au>Shin, Joo-Ho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2016-05-01</date><risdate>2016</risdate><volume>41</volume><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><abstract>Abstract During normal aging, the number of dopaminergic (DA) neurons in the substantia nigra (SN) progressively diminishes, while massive DA neuronal loss is a hallmark sign of Parkinson’s disease (PD). Unfortunately, there is little known about the molecular events involved in age-related DA neuronal loss. In this study, we found that (1) the level of parkin was decreased in the cerebellum, brain stem, SN, and striatum of aged mice, (2) diaminodiphenyl sulfone (DDS) restored the level of parkin, (3) DDS prevented age-dependent DA neuronal loss, and (4) DDS protected SH-SY5Y cells from MPP+ and H2 O2 . Furthermore, pre/post-treatment of DDS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model attenuated DA neuronal loss and restored motor behavior. DDS transcriptionally activated parkin via PERK-ATF4 signaling and DDS not only failed to induce parkin expression, but also failed to rescue SH-SY5Y cells from MPP+ in the absence of ATF4. Herein, we demonstrated for the first time that DDS increased parkin level and served as a neuroprotective agent for age-dependent DA neuronal loss. Thus, DDS may be a potential therapeutic agent for age-related neurodegeneration.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27103513</pmid><doi>10.1016/j.neurobiolaging.2015.11.008</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-0425-3377</orcidid><orcidid>https://orcid.org/0000-0002-0499-4589</orcidid></addata></record> |
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| ispartof | Neurobiology of aging, 2016-05, Vol.41, p.1-10 |
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| subjects | Activating Transcription Factor 4 - physiology Aging Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Brain - metabolism Cells, Cultured Dapsone - pharmacology Dapsone - therapeutic use Diaminodiphenyl sulfone Disease Models, Animal Dopaminergic neuron Dopaminergic Neurons - pathology eIF-2 Kinase - physiology Endoplasmic Reticulum Stress ER stress Female Internal Medicine Male Mice, Inbred C57BL Neurology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Parkin Parkinson Disease - drug therapy Parkinson Disease - pathology Parkinson's disease PERK-ATF4 signaling Signal Transduction - drug effects Signal Transduction - physiology Substantia Nigra - cytology Substantia Nigra - pathology Ubiquitin-Protein Ligases - deficiency Ubiquitin-Protein Ligases - metabolism |
| title | Diaminodiphenyl sulfone-induced parkin ameliorates age-dependent dopaminergic neuronal loss |
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