Mitochondrial dysfunction is implicated in retinoic acid-induced spina bifida aperta in rat fetuses
Neural tube defects (NTDs) are the most common and severe congenital malformations, which result from failure of the neural tube to close during embryonic development. The etiology of NTDs is complex, caused by interactions between genetic defects and environmental factors, but the exact mechanisms...
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| Veröffentlicht in: | International journal of developmental neuroscience 2018-08, Vol.68 (1), p.39-44 |
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| container_title | International journal of developmental neuroscience |
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| creator | Xue, Jia Gu, Hui Liu, Dan Ma, Wei Wei, Xiaowei Zhao, Lianshuai Liu, Yusi Zhang, Chaonan Yuan, Zhengwei |
| description | Neural tube defects (NTDs) are the most common and severe congenital malformations, which result from failure of the neural tube to close during embryonic development. The etiology of NTDs is complex, caused by interactions between genetic defects and environmental factors, but the exact mechanisms of this disease are still not fully understood. We herein employ a Seahorse Bioscience microplate-based extracellular flux (XF) analyzer to determine mitochondrial function and quantify respiratory coupling to various bioenergetic functions using specific pharmacological inhibitors of bioenergetic pathways. We demonstrate that changes in coupling between ATP turnover and proton leak are correlated with NTDs. Further, we determined that the ATP content and oxidative stress levels in posterior spinal cords of rat embryos with NTDs between E11 and E14 was lower than that of normal controls. The present study reveals that mitochondrial dysfunction is associated with all-trans retinoic acid (atRA)-induced NTDs in rat embryos. Oxidative stress results from decreased antioxidant enzyme activity. This study provides a novel viewpoint for exploring the embryonic pathogenesis of atRA-induced NTDs. |
| doi_str_mv | 10.1016/j.ijdevneu.2018.04.003 |
| format | Article |
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The etiology of NTDs is complex, caused by interactions between genetic defects and environmental factors, but the exact mechanisms of this disease are still not fully understood. We herein employ a Seahorse Bioscience microplate-based extracellular flux (XF) analyzer to determine mitochondrial function and quantify respiratory coupling to various bioenergetic functions using specific pharmacological inhibitors of bioenergetic pathways. We demonstrate that changes in coupling between ATP turnover and proton leak are correlated with NTDs. Further, we determined that the ATP content and oxidative stress levels in posterior spinal cords of rat embryos with NTDs between E11 and E14 was lower than that of normal controls. The present study reveals that mitochondrial dysfunction is associated with all-trans retinoic acid (atRA)-induced NTDs in rat embryos. Oxidative stress results from decreased antioxidant enzyme activity. This study provides a novel viewpoint for exploring the embryonic pathogenesis of atRA-induced NTDs.</description><identifier>ISSN: 0736-5748</identifier><identifier>EISSN: 1873-474X</identifier><identifier>DOI: 10.1016/j.ijdevneu.2018.04.003</identifier><identifier>PMID: 29689339</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Adenosine Triphosphate - metabolism ; Age Factors ; All-trans retinoic acid ; Animals ; Antioxidants ; Bioenergetics ; Catalase - metabolism ; Congenital defects ; Cords ; Coupling ; Cyclooxygenase 1 - metabolism ; Defects ; Embryo, Mammalian ; Embryogenesis ; Embryonic growth stage ; Embryos ; Energy metabolism ; Environmental factors ; Enzymatic activity ; Enzyme activity ; Etiology ; Fetuses ; Gene Expression Regulation, Enzymologic - drug effects ; Keratolytic Agents - toxicity ; Lipid Peroxidation - drug effects ; Mitochondria ; Mitochondrial Diseases - etiology ; Mitochondrial dysfunction ; Neural tube defects ; Oxidative stress ; Oxygen Consumption - drug effects ; Pathogenesis ; Pharmacology ; Rats ; Rats, Wistar ; Retinoic acid ; Rodents ; Spina bifida ; Spina Bifida Cystica - chemically induced ; Spina Bifida Cystica - complications ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Superoxide Dismutase - metabolism ; Tretinoin - toxicity</subject><ispartof>International journal of developmental neuroscience, 2018-08, Vol.68 (1), p.39-44</ispartof><rights>2018 ISDN</rights><rights>Copyright © 2018 ISDN. Published by Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier BV Aug 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4623-72e3b4b3bba7586601a28c1baad3ef6f5d1af4277e31ef6c95c1e3084f31d073</citedby><cites>FETCH-LOGICAL-c4623-72e3b4b3bba7586601a28c1baad3ef6f5d1af4277e31ef6c95c1e3084f31d073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.ijdevneu.2018.04.003$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1016%2Fj.ijdevneu.2018.04.003$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29689339$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xue, Jia</creatorcontrib><creatorcontrib>Gu, Hui</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Wei, Xiaowei</creatorcontrib><creatorcontrib>Zhao, Lianshuai</creatorcontrib><creatorcontrib>Liu, Yusi</creatorcontrib><creatorcontrib>Zhang, Chaonan</creatorcontrib><creatorcontrib>Yuan, Zhengwei</creatorcontrib><title>Mitochondrial dysfunction is implicated in retinoic acid-induced spina bifida aperta in rat fetuses</title><title>International journal of developmental neuroscience</title><addtitle>Int J Dev Neurosci</addtitle><description>Neural tube defects (NTDs) are the most common and severe congenital malformations, which result from failure of the neural tube to close during embryonic development. The etiology of NTDs is complex, caused by interactions between genetic defects and environmental factors, but the exact mechanisms of this disease are still not fully understood. We herein employ a Seahorse Bioscience microplate-based extracellular flux (XF) analyzer to determine mitochondrial function and quantify respiratory coupling to various bioenergetic functions using specific pharmacological inhibitors of bioenergetic pathways. We demonstrate that changes in coupling between ATP turnover and proton leak are correlated with NTDs. Further, we determined that the ATP content and oxidative stress levels in posterior spinal cords of rat embryos with NTDs between E11 and E14 was lower than that of normal controls. The present study reveals that mitochondrial dysfunction is associated with all-trans retinoic acid (atRA)-induced NTDs in rat embryos. Oxidative stress results from decreased antioxidant enzyme activity. This study provides a novel viewpoint for exploring the embryonic pathogenesis of atRA-induced NTDs.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Age Factors</subject><subject>All-trans retinoic acid</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Bioenergetics</subject><subject>Catalase - metabolism</subject><subject>Congenital defects</subject><subject>Cords</subject><subject>Coupling</subject><subject>Cyclooxygenase 1 - metabolism</subject><subject>Defects</subject><subject>Embryo, Mammalian</subject><subject>Embryogenesis</subject><subject>Embryonic growth stage</subject><subject>Embryos</subject><subject>Energy metabolism</subject><subject>Environmental factors</subject><subject>Enzymatic activity</subject><subject>Enzyme activity</subject><subject>Etiology</subject><subject>Fetuses</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Keratolytic Agents - toxicity</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Mitochondria</subject><subject>Mitochondrial Diseases - etiology</subject><subject>Mitochondrial dysfunction</subject><subject>Neural tube defects</subject><subject>Oxidative stress</subject><subject>Oxygen Consumption - drug effects</subject><subject>Pathogenesis</subject><subject>Pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Retinoic acid</subject><subject>Rodents</subject><subject>Spina bifida</subject><subject>Spina Bifida Cystica - chemically induced</subject><subject>Spina Bifida Cystica - complications</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Tretinoin - toxicity</subject><issn>0736-5748</issn><issn>1873-474X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EokvhL1SRuHBJ8Fe-bqB2gV2VcimIm-XYYzFR1gl20mr_PV7ScuACJ2vsZ17PvC8hF4wWjLLqbV9gb-HOw1JwypqCyoJS8YRsWFOLXNby-1OyobWo8rKWzRl5EWNPKS1LKp-TM95WTStEuyHmM86j-TF6G1APmT1Gt3gz4-gzjBkepgGNnsFm6LMAM_oRTaYN2hy9XUx6iBN6nXXo0OpMTxBm_RvWc-ZgXiLEl-SZ00OEVw_nObn9sL29_JRff_m4u3x_nRtZcZHXHEQnO9F1ui6bqqJM88awTmsrwFWutEw7yesaBEu1aUvDQNBGOsFsWvWcvFllpzD-XCDO6oDRwDBoD-MSFaeCtoxXXCb09V9oPy7Bp-ES1fKmTU6dBKuVMmGMMYBTU8CDDkfFqDqloHr1mII6paCoVCmF1HjxIL90B7B_2h5tT8BuBe5xgON_yqr91c1-t7_afrvZfj3dU7l-9m7VgmTtHUJQ0SD4FA0GMLOyI_5r3l-KXrOY</recordid><startdate>201808</startdate><enddate>201808</enddate><creator>Xue, Jia</creator><creator>Gu, Hui</creator><creator>Liu, Dan</creator><creator>Ma, Wei</creator><creator>Wei, Xiaowei</creator><creator>Zhao, Lianshuai</creator><creator>Liu, Yusi</creator><creator>Zhang, Chaonan</creator><creator>Yuan, Zhengwei</creator><general>Elsevier Ltd</general><general>Elsevier BV</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201808</creationdate><title>Mitochondrial dysfunction is implicated in retinoic acid-induced spina bifida aperta in rat fetuses</title><author>Xue, Jia ; Gu, Hui ; Liu, Dan ; Ma, Wei ; Wei, Xiaowei ; Zhao, Lianshuai ; Liu, Yusi ; Zhang, Chaonan ; Yuan, Zhengwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4623-72e3b4b3bba7586601a28c1baad3ef6f5d1af4277e31ef6c95c1e3084f31d073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Age Factors</topic><topic>All-trans retinoic acid</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Bioenergetics</topic><topic>Catalase - metabolism</topic><topic>Congenital defects</topic><topic>Cords</topic><topic>Coupling</topic><topic>Cyclooxygenase 1 - metabolism</topic><topic>Defects</topic><topic>Embryo, Mammalian</topic><topic>Embryogenesis</topic><topic>Embryonic growth stage</topic><topic>Embryos</topic><topic>Energy metabolism</topic><topic>Environmental factors</topic><topic>Enzymatic activity</topic><topic>Enzyme activity</topic><topic>Etiology</topic><topic>Fetuses</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>Keratolytic Agents - toxicity</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Mitochondria</topic><topic>Mitochondrial Diseases - etiology</topic><topic>Mitochondrial dysfunction</topic><topic>Neural tube defects</topic><topic>Oxidative stress</topic><topic>Oxygen Consumption - drug effects</topic><topic>Pathogenesis</topic><topic>Pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Retinoic acid</topic><topic>Rodents</topic><topic>Spina bifida</topic><topic>Spina Bifida Cystica - chemically induced</topic><topic>Spina Bifida Cystica - complications</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tretinoin - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xue, Jia</creatorcontrib><creatorcontrib>Gu, Hui</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Ma, Wei</creatorcontrib><creatorcontrib>Wei, Xiaowei</creatorcontrib><creatorcontrib>Zhao, Lianshuai</creatorcontrib><creatorcontrib>Liu, Yusi</creatorcontrib><creatorcontrib>Zhang, Chaonan</creatorcontrib><creatorcontrib>Yuan, Zhengwei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of developmental neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xue, Jia</au><au>Gu, Hui</au><au>Liu, Dan</au><au>Ma, Wei</au><au>Wei, Xiaowei</au><au>Zhao, Lianshuai</au><au>Liu, Yusi</au><au>Zhang, Chaonan</au><au>Yuan, Zhengwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial dysfunction is implicated in retinoic acid-induced spina bifida aperta in rat fetuses</atitle><jtitle>International journal of developmental neuroscience</jtitle><addtitle>Int J Dev Neurosci</addtitle><date>2018-08</date><risdate>2018</risdate><volume>68</volume><issue>1</issue><spage>39</spage><epage>44</epage><pages>39-44</pages><issn>0736-5748</issn><eissn>1873-474X</eissn><abstract>Neural tube defects (NTDs) are the most common and severe congenital malformations, which result from failure of the neural tube to close during embryonic development. The etiology of NTDs is complex, caused by interactions between genetic defects and environmental factors, but the exact mechanisms of this disease are still not fully understood. We herein employ a Seahorse Bioscience microplate-based extracellular flux (XF) analyzer to determine mitochondrial function and quantify respiratory coupling to various bioenergetic functions using specific pharmacological inhibitors of bioenergetic pathways. We demonstrate that changes in coupling between ATP turnover and proton leak are correlated with NTDs. Further, we determined that the ATP content and oxidative stress levels in posterior spinal cords of rat embryos with NTDs between E11 and E14 was lower than that of normal controls. The present study reveals that mitochondrial dysfunction is associated with all-trans retinoic acid (atRA)-induced NTDs in rat embryos. Oxidative stress results from decreased antioxidant enzyme activity. This study provides a novel viewpoint for exploring the embryonic pathogenesis of atRA-induced NTDs.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>29689339</pmid><doi>10.1016/j.ijdevneu.2018.04.003</doi><tpages>6</tpages></addata></record> |
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| subjects | Adenosine Triphosphate - metabolism Age Factors All-trans retinoic acid Animals Antioxidants Bioenergetics Catalase - metabolism Congenital defects Cords Coupling Cyclooxygenase 1 - metabolism Defects Embryo, Mammalian Embryogenesis Embryonic growth stage Embryos Energy metabolism Environmental factors Enzymatic activity Enzyme activity Etiology Fetuses Gene Expression Regulation, Enzymologic - drug effects Keratolytic Agents - toxicity Lipid Peroxidation - drug effects Mitochondria Mitochondrial Diseases - etiology Mitochondrial dysfunction Neural tube defects Oxidative stress Oxygen Consumption - drug effects Pathogenesis Pharmacology Rats Rats, Wistar Retinoic acid Rodents Spina bifida Spina Bifida Cystica - chemically induced Spina Bifida Cystica - complications Spinal Cord - drug effects Spinal Cord - metabolism Superoxide Dismutase - metabolism Tretinoin - toxicity |
| title | Mitochondrial dysfunction is implicated in retinoic acid-induced spina bifida aperta in rat fetuses |
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