Melatonin protected against the detrimental effects of microRNA‐363 in a rat model of vitamin A‐associated congenital spinal deformities: Involvement of Notch signaling
Congenital spinal deformities are a result of defective somitogenesis and are associated with vitamin A deficiency (VAD). However, the molecular mechanisms of VAD‐associated congenital spinal deformities remain largely unknown. Increasing number of studies suggested that microRNAs and melatonin play...
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| Veröffentlicht in: | Journal of pineal research 2019-04, Vol.66 (3), p.e12558-n/a |
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| container_title | Journal of pineal research |
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| creator | Li, Zheng Li, Xingye Bi, Jiaqi Chan, Matthew T. V. Wu, William Ka Kei Shen, Jianxiong |
| description | Congenital spinal deformities are a result of defective somitogenesis and are associated with vitamin A deficiency (VAD). However, the molecular mechanisms of VAD‐associated congenital spinal deformities remain largely unknown. Increasing number of studies suggested that microRNAs and melatonin played important roles in the development of congenital spinal deformities. In this study, we showed that the whole‐embryo expression of miR‐363 was upregulated in VAD rats. Furthermore, we demonstrated that miR‐363 inhibited the proliferation and neuronal differentiation of primary cultured NSCs, accompanied by downregulation of Notch1. To this end, melatonin suppressed miR‐363 expression and rescued the effects of miR‐363 on NSC proliferation and neuronal differentiation together with restoration of Notch signaling. The present study provided new insights into the mechanism of VAD‐associated spinal deformities and the therapeutic effect of melatonin that may lead to novel understanding of the molecular mechanisms of congenital spinal deformities. |
| doi_str_mv | 10.1111/jpi.12558 |
| format | Article |
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V. ; Wu, William Ka Kei ; Shen, Jianxiong</creator><creatorcontrib>Li, Zheng ; Li, Xingye ; Bi, Jiaqi ; Chan, Matthew T. V. ; Wu, William Ka Kei ; Shen, Jianxiong</creatorcontrib><description>Congenital spinal deformities are a result of defective somitogenesis and are associated with vitamin A deficiency (VAD). However, the molecular mechanisms of VAD‐associated congenital spinal deformities remain largely unknown. Increasing number of studies suggested that microRNAs and melatonin played important roles in the development of congenital spinal deformities. In this study, we showed that the whole‐embryo expression of miR‐363 was upregulated in VAD rats. Furthermore, we demonstrated that miR‐363 inhibited the proliferation and neuronal differentiation of primary cultured NSCs, accompanied by downregulation of Notch1. To this end, melatonin suppressed miR‐363 expression and rescued the effects of miR‐363 on NSC proliferation and neuronal differentiation together with restoration of Notch signaling. The present study provided new insights into the mechanism of VAD‐associated spinal deformities and the therapeutic effect of melatonin that may lead to novel understanding of the molecular mechanisms of congenital spinal deformities.</description><identifier>ISSN: 0742-3098</identifier><identifier>EISSN: 1600-079X</identifier><identifier>DOI: 10.1111/jpi.12558</identifier><identifier>PMID: 30653707</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell Proliferation - drug effects ; Cell Proliferation - genetics ; congenital spinal deformities ; Disease Models, Animal ; Female ; melatonin ; Melatonin - pharmacology ; MicroRNAs - genetics ; miR‐363 ; Neural Stem Cells - drug effects ; Neural Stem Cells - metabolism ; Neurogenesis - drug effects ; Neurogenesis - genetics ; Notch1 ; Rats ; Rats, Wistar ; Receptor, Notch1 - metabolism ; Signal Transduction - drug effects ; Spinal Dysraphism - etiology ; Spinal Dysraphism - genetics ; Spinal Dysraphism - metabolism ; vitamin A deficiency ; Vitamin A Deficiency - complications</subject><ispartof>Journal of pineal research, 2019-04, Vol.66 (3), p.e12558-n/a</ispartof><rights>2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3258-deba5d324364ea62b2a81bb600f2467ff0d1e6d7d9d70339b52fcd3f626210333</citedby><cites>FETCH-LOGICAL-c3258-deba5d324364ea62b2a81bb600f2467ff0d1e6d7d9d70339b52fcd3f626210333</cites><orcidid>0000-0001-5449-6740</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjpi.12558$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjpi.12558$$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/30653707$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Zheng</creatorcontrib><creatorcontrib>Li, Xingye</creatorcontrib><creatorcontrib>Bi, Jiaqi</creatorcontrib><creatorcontrib>Chan, Matthew T. V.</creatorcontrib><creatorcontrib>Wu, William Ka Kei</creatorcontrib><creatorcontrib>Shen, Jianxiong</creatorcontrib><title>Melatonin protected against the detrimental effects of microRNA‐363 in a rat model of vitamin A‐associated congenital spinal deformities: Involvement of Notch signaling</title><title>Journal of pineal research</title><addtitle>J Pineal Res</addtitle><description>Congenital spinal deformities are a result of defective somitogenesis and are associated with vitamin A deficiency (VAD). However, the molecular mechanisms of VAD‐associated congenital spinal deformities remain largely unknown. Increasing number of studies suggested that microRNAs and melatonin played important roles in the development of congenital spinal deformities. In this study, we showed that the whole‐embryo expression of miR‐363 was upregulated in VAD rats. Furthermore, we demonstrated that miR‐363 inhibited the proliferation and neuronal differentiation of primary cultured NSCs, accompanied by downregulation of Notch1. To this end, melatonin suppressed miR‐363 expression and rescued the effects of miR‐363 on NSC proliferation and neuronal differentiation together with restoration of Notch signaling. The present study provided new insights into the mechanism of VAD‐associated spinal deformities and the therapeutic effect of melatonin that may lead to novel understanding of the molecular mechanisms of congenital spinal deformities.</description><subject>Animals</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - genetics</subject><subject>congenital spinal deformities</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>melatonin</subject><subject>Melatonin - pharmacology</subject><subject>MicroRNAs - genetics</subject><subject>miR‐363</subject><subject>Neural Stem Cells - drug effects</subject><subject>Neural Stem Cells - metabolism</subject><subject>Neurogenesis - drug effects</subject><subject>Neurogenesis - genetics</subject><subject>Notch1</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Notch1 - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Spinal Dysraphism - etiology</subject><subject>Spinal Dysraphism - genetics</subject><subject>Spinal Dysraphism - metabolism</subject><subject>vitamin A deficiency</subject><subject>Vitamin A Deficiency - complications</subject><issn>0742-3098</issn><issn>1600-079X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc2O0zAURi0Eop3CghdAXsIirX8SJ2E3GsFMUSkIgcQucuLr1FVid2K3qDsegQeZp-JJcEhhhzdXujr3WPo-hF5QsqTxrfYHs6Qsy4pHaE4FIQnJy2-P0ZzkKUs4KYsZuvJ-TwgpikI8RTNORMZzks_RwwfoZHDWWHwYXIAmgMKylcb6gMMOsIIwmB5skB0GrSPgsdO4N83gPm-vf_34yQXH8VziQQbcOwXdCJxMkH1cj4T03jVGjurG2RasGW3-YGwcCrQbehMM-Dd4bU-uO8H43yjZutDssDdtBI1tn6EnWnYenl_mAn199_bLzV2y-Xi7vrneJA1nWZEoqGWmOEu5SEEKVjNZ0LqOwWiWilxroigIlatS5YTzss6YbhTXgglG44Iv0KvJGyO5P4IPVW98A10nLbijrxjNy5QQUWQRfT2hMQ7vB9DVIcYlh3NFSTWWU8Vyqj_lRPblRXuse1D_yL9tRGA1Ad9NB-f_m6r3n9aT8jcVJZ3N</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Li, Zheng</creator><creator>Li, Xingye</creator><creator>Bi, Jiaqi</creator><creator>Chan, Matthew T. V.</creator><creator>Wu, William Ka Kei</creator><creator>Shen, Jianxiong</creator><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><orcidid>https://orcid.org/0000-0001-5449-6740</orcidid></search><sort><creationdate>201904</creationdate><title>Melatonin protected against the detrimental effects of microRNA‐363 in a rat model of vitamin A‐associated congenital spinal deformities: Involvement of Notch signaling</title><author>Li, Zheng ; Li, Xingye ; Bi, Jiaqi ; Chan, Matthew T. V. ; Wu, William Ka Kei ; Shen, Jianxiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3258-deba5d324364ea62b2a81bb600f2467ff0d1e6d7d9d70339b52fcd3f626210333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - genetics</topic><topic>congenital spinal deformities</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>melatonin</topic><topic>Melatonin - pharmacology</topic><topic>MicroRNAs - genetics</topic><topic>miR‐363</topic><topic>Neural Stem Cells - drug effects</topic><topic>Neural Stem Cells - metabolism</topic><topic>Neurogenesis - drug effects</topic><topic>Neurogenesis - genetics</topic><topic>Notch1</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Notch1 - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Spinal Dysraphism - etiology</topic><topic>Spinal Dysraphism - genetics</topic><topic>Spinal Dysraphism - metabolism</topic><topic>vitamin A deficiency</topic><topic>Vitamin A Deficiency - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Zheng</creatorcontrib><creatorcontrib>Li, Xingye</creatorcontrib><creatorcontrib>Bi, Jiaqi</creatorcontrib><creatorcontrib>Chan, Matthew T. 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In this study, we showed that the whole‐embryo expression of miR‐363 was upregulated in VAD rats. Furthermore, we demonstrated that miR‐363 inhibited the proliferation and neuronal differentiation of primary cultured NSCs, accompanied by downregulation of Notch1. To this end, melatonin suppressed miR‐363 expression and rescued the effects of miR‐363 on NSC proliferation and neuronal differentiation together with restoration of Notch signaling. The present study provided new insights into the mechanism of VAD‐associated spinal deformities and the therapeutic effect of melatonin that may lead to novel understanding of the molecular mechanisms of congenital spinal deformities.</abstract><cop>England</cop><pmid>30653707</pmid><doi>10.1111/jpi.12558</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-5449-6740</orcidid></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Cell Differentiation - drug effects Cell Differentiation - genetics Cell Proliferation - drug effects Cell Proliferation - genetics congenital spinal deformities Disease Models, Animal Female melatonin Melatonin - pharmacology MicroRNAs - genetics miR‐363 Neural Stem Cells - drug effects Neural Stem Cells - metabolism Neurogenesis - drug effects Neurogenesis - genetics Notch1 Rats Rats, Wistar Receptor, Notch1 - metabolism Signal Transduction - drug effects Spinal Dysraphism - etiology Spinal Dysraphism - genetics Spinal Dysraphism - metabolism vitamin A deficiency Vitamin A Deficiency - complications |
| title | Melatonin protected against the detrimental effects of microRNA‐363 in a rat model of vitamin A‐associated congenital spinal deformities: Involvement of Notch signaling |
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