The Mitochondrial-Derived Peptide (MOTS-c) Interacted with Nrf2 to Defend the Antioxidant System to Protect Dopaminergic Neurons Against Rotenone Exposure
MOTS-c is a 16-amino acid mitochondrial-derived peptide reported to be involved in regulating energy metabolism. However, few studies have reported the role of MOTS-c on neuron degeneration. In this study, it was aimed to explore the action of MOTS-c in rotenone-induced dopaminergic neurotoxicity. I...
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| Veröffentlicht in: | Molecular neurobiology 2023-10, Vol.60 (10), p.5915-5930 |
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| creator | Xiao, Jingsong Zhang, Qifu Shan, Yaohui Ye, Feng Zhang, Xi Cheng, Jin Wang, Xiaogang Zhao, Yuanpeng Dan, Guorong Chen, Mingliang Sai, Yan |
| description | MOTS-c is a 16-amino acid mitochondrial-derived peptide reported to be involved in regulating energy metabolism. However, few studies have reported the role of MOTS-c on neuron degeneration. In this study, it was aimed to explore the action of MOTS-c in rotenone-induced dopaminergic neurotoxicity. In an in vitro study, it was observed that rotenone could influence the expression and localization of MOTS-c significantly in PC12 cells, with more MOTS-c translocating into the nucleus from mitochondria. Further study showed that the translocation of MOTS-c from the mitochondria into the nucleus could directly interact with Nrf2 to regulate HO-1 and NQO1 expression in PC12 cells exposed to rotenone, which had been suggested to be involved in the antioxidant defense system. In vivo and in vitro experiments demonstrated that exogenous MOTS-c pretreatment could protect PC12 cells and rats from mitochondrial dysfunction and oxidative stress induced by rotenone. Moreover, MOTS-c pretreatment significantly decreased the loss of TH, PSD95, and SYP protein expression in the striatum of rats exposed to rotenone. In addition, MOTS-c pretreatment could clearly alleviate the downregulated expression of Nrf2, HO-1, and NQO1, as well as the upregulated Keap1 protein expression in the striatum of rotenone-treated rats. Taken together, these findings suggested that MOTS-c could directly interact with Nrf2 to activate the Nrf2/HO-1/NQO1 signal pathway to defend the antioxidant system to prevent dopaminergic neurons from rotenone-induced oxidative stress and neurotoxicity in vitro and in vivo. |
| doi_str_mv | 10.1007/s12035-023-03443-3 |
| format | Article |
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However, few studies have reported the role of MOTS-c on neuron degeneration. In this study, it was aimed to explore the action of MOTS-c in rotenone-induced dopaminergic neurotoxicity. In an in vitro study, it was observed that rotenone could influence the expression and localization of MOTS-c significantly in PC12 cells, with more MOTS-c translocating into the nucleus from mitochondria. Further study showed that the translocation of MOTS-c from the mitochondria into the nucleus could directly interact with Nrf2 to regulate HO-1 and NQO1 expression in PC12 cells exposed to rotenone, which had been suggested to be involved in the antioxidant defense system. In vivo and in vitro experiments demonstrated that exogenous MOTS-c pretreatment could protect PC12 cells and rats from mitochondrial dysfunction and oxidative stress induced by rotenone. Moreover, MOTS-c pretreatment significantly decreased the loss of TH, PSD95, and SYP protein expression in the striatum of rats exposed to rotenone. In addition, MOTS-c pretreatment could clearly alleviate the downregulated expression of Nrf2, HO-1, and NQO1, as well as the upregulated Keap1 protein expression in the striatum of rotenone-treated rats. Taken together, these findings suggested that MOTS-c could directly interact with Nrf2 to activate the Nrf2/HO-1/NQO1 signal pathway to defend the antioxidant system to prevent dopaminergic neurons from rotenone-induced oxidative stress and neurotoxicity in vitro and in vivo.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-023-03443-3</identifier><identifier>PMID: 37380822</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Amino acids ; Antioxidants ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Dopamine receptors ; Energy metabolism ; Localization ; Mitochondria ; Neostriatum ; Neurobiology ; Neurology ; Neurosciences ; Neurotoxicity ; Oxidative stress ; Peptides ; Pheochromocytoma cells ; Postsynaptic density proteins ; Protein expression ; Rotenone ; Syp protein</subject><ispartof>Molecular neurobiology, 2023-10, Vol.60 (10), p.5915-5930</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. 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The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-4d4dd15133ff828e2bcbe526797324af17c45563e0bd762605c3c5f2ddbead893</citedby><cites>FETCH-LOGICAL-c375t-4d4dd15133ff828e2bcbe526797324af17c45563e0bd762605c3c5f2ddbead893</cites><orcidid>0000-0002-5520-0443</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-023-03443-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-023-03443-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27913,27914,41477,42546,51308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37380822$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Jingsong</creatorcontrib><creatorcontrib>Zhang, Qifu</creatorcontrib><creatorcontrib>Shan, Yaohui</creatorcontrib><creatorcontrib>Ye, Feng</creatorcontrib><creatorcontrib>Zhang, Xi</creatorcontrib><creatorcontrib>Cheng, Jin</creatorcontrib><creatorcontrib>Wang, Xiaogang</creatorcontrib><creatorcontrib>Zhao, Yuanpeng</creatorcontrib><creatorcontrib>Dan, Guorong</creatorcontrib><creatorcontrib>Chen, Mingliang</creatorcontrib><creatorcontrib>Sai, Yan</creatorcontrib><title>The Mitochondrial-Derived Peptide (MOTS-c) Interacted with Nrf2 to Defend the Antioxidant System to Protect Dopaminergic Neurons Against Rotenone Exposure</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>MOTS-c is a 16-amino acid mitochondrial-derived peptide reported to be involved in regulating energy metabolism. However, few studies have reported the role of MOTS-c on neuron degeneration. In this study, it was aimed to explore the action of MOTS-c in rotenone-induced dopaminergic neurotoxicity. In an in vitro study, it was observed that rotenone could influence the expression and localization of MOTS-c significantly in PC12 cells, with more MOTS-c translocating into the nucleus from mitochondria. Further study showed that the translocation of MOTS-c from the mitochondria into the nucleus could directly interact with Nrf2 to regulate HO-1 and NQO1 expression in PC12 cells exposed to rotenone, which had been suggested to be involved in the antioxidant defense system. In vivo and in vitro experiments demonstrated that exogenous MOTS-c pretreatment could protect PC12 cells and rats from mitochondrial dysfunction and oxidative stress induced by rotenone. Moreover, MOTS-c pretreatment significantly decreased the loss of TH, PSD95, and SYP protein expression in the striatum of rats exposed to rotenone. In addition, MOTS-c pretreatment could clearly alleviate the downregulated expression of Nrf2, HO-1, and NQO1, as well as the upregulated Keap1 protein expression in the striatum of rotenone-treated rats. Taken together, these findings suggested that MOTS-c could directly interact with Nrf2 to activate the Nrf2/HO-1/NQO1 signal pathway to defend the antioxidant system to prevent dopaminergic neurons from rotenone-induced oxidative stress and neurotoxicity in vitro and in vivo.</description><subject>Amino acids</subject><subject>Antioxidants</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Dopamine receptors</subject><subject>Energy metabolism</subject><subject>Localization</subject><subject>Mitochondria</subject><subject>Neostriatum</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Oxidative stress</subject><subject>Peptides</subject><subject>Pheochromocytoma cells</subject><subject>Postsynaptic density proteins</subject><subject>Protein expression</subject><subject>Rotenone</subject><subject>Syp 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(MOTS-c) Interacted with Nrf2 to Defend the Antioxidant System to Protect Dopaminergic Neurons Against Rotenone Exposure</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>60</volume><issue>10</issue><spage>5915</spage><epage>5930</epage><pages>5915-5930</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>MOTS-c is a 16-amino acid mitochondrial-derived peptide reported to be involved in regulating energy metabolism. However, few studies have reported the role of MOTS-c on neuron degeneration. In this study, it was aimed to explore the action of MOTS-c in rotenone-induced dopaminergic neurotoxicity. In an in vitro study, it was observed that rotenone could influence the expression and localization of MOTS-c significantly in PC12 cells, with more MOTS-c translocating into the nucleus from mitochondria. Further study showed that the translocation of MOTS-c from the mitochondria into the nucleus could directly interact with Nrf2 to regulate HO-1 and NQO1 expression in PC12 cells exposed to rotenone, which had been suggested to be involved in the antioxidant defense system. In vivo and in vitro experiments demonstrated that exogenous MOTS-c pretreatment could protect PC12 cells and rats from mitochondrial dysfunction and oxidative stress induced by rotenone. Moreover, MOTS-c pretreatment significantly decreased the loss of TH, PSD95, and SYP protein expression in the striatum of rats exposed to rotenone. In addition, MOTS-c pretreatment could clearly alleviate the downregulated expression of Nrf2, HO-1, and NQO1, as well as the upregulated Keap1 protein expression in the striatum of rotenone-treated rats. Taken together, these findings suggested that MOTS-c could directly interact with Nrf2 to activate the Nrf2/HO-1/NQO1 signal pathway to defend the antioxidant system to prevent dopaminergic neurons from rotenone-induced oxidative stress and neurotoxicity in vitro and in vivo.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37380822</pmid><doi>10.1007/s12035-023-03443-3</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-5520-0443</orcidid></addata></record> |
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| subjects | Amino acids Antioxidants Biomedical and Life Sciences Biomedicine Cell Biology Dopamine receptors Energy metabolism Localization Mitochondria Neostriatum Neurobiology Neurology Neurosciences Neurotoxicity Oxidative stress Peptides Pheochromocytoma cells Postsynaptic density proteins Protein expression Rotenone Syp protein |
| title | The Mitochondrial-Derived Peptide (MOTS-c) Interacted with Nrf2 to Defend the Antioxidant System to Protect Dopaminergic Neurons Against Rotenone Exposure |
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