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Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease
Perturbation in apoptosis can lead to Hirschsprung's disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic...
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Published in: | International journal of nanomedicine 2016, Vol.11, p.5871-5881 |
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container_title | International journal of nanomedicine |
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description | Perturbation in apoptosis can lead to Hirschsprung's disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR. |
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It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR.</description><identifier>ISSN: 1178-2013</identifier><identifier>ISSN: 1176-9114</identifier><identifier>EISSN: 1178-2013</identifier><identifier>DOI: 10.2147/IJN.S114838</identifier><identifier>PMID: 27853370</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>Adenosine Triphosphate - metabolism ; Alzheimer's disease ; Apoptosis ; Apoptosis - genetics ; Biomarkers - metabolism ; Cancer ; Case-Control Studies ; Cell adhesion & migration ; Cell Line ; Colon - pathology ; Congenital diseases ; Cytochrome c ; Cytochromes c - metabolism ; Exosomal long non-coding RNA ; Exosomes - metabolism ; Experiments ; Female ; Gene Expression Regulation ; Hirschsprung disease ; Hirschsprung Disease - diagnosis ; Hirschsprung Disease - genetics ; Hirschsprung Disease - pathology ; Humans ; Infant, Newborn ; Intercellular communication ; Laboratories ; Male ; MicroRNAs ; Microscopy ; Mitochondria ; Mitochondria - genetics ; Mitochondria - pathology ; Nervous system ; Neuronal development ; Neurons ; Neurons - metabolism ; Neurons - pathology ; Original Research ; Pediatrics ; Peptides ; Proteins - chemistry ; Proteins - genetics ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Stem cells ; Surgery ; Toxicology</subject><ispartof>International journal of nanomedicine, 2016, Vol.11, p.5871-5881</ispartof><rights>COPYRIGHT 2016 Dove Medical Press Limited</rights><rights>2016. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Du et al. This work is published and licensed by Dove Medical Press Limited 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-662b512d612f93b6f218070aaa5a3dc784b30e95402fa6fea0ebbc0d1dfe92543</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2240103524/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2240103524?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,25753,27923,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27853370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Chunxia</creatorcontrib><creatorcontrib>Xie, Hua</creatorcontrib><creatorcontrib>Zang, Rujin</creatorcontrib><creatorcontrib>Shen, Ziyang</creatorcontrib><creatorcontrib>Li, Hongxing</creatorcontrib><creatorcontrib>Chen, Pingfa</creatorcontrib><creatorcontrib>Xu, Xiaoqun</creatorcontrib><creatorcontrib>Xia, Yankai</creatorcontrib><creatorcontrib>Tang, Weibing</creatorcontrib><title>Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease</title><title>International journal of nanomedicine</title><addtitle>Int J Nanomedicine</addtitle><description>Perturbation in apoptosis can lead to Hirschsprung's disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Alzheimer's disease</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biomarkers - metabolism</subject><subject>Cancer</subject><subject>Case-Control Studies</subject><subject>Cell adhesion & migration</subject><subject>Cell Line</subject><subject>Colon - pathology</subject><subject>Congenital diseases</subject><subject>Cytochrome c</subject><subject>Cytochromes c - metabolism</subject><subject>Exosomal long non-coding RNA</subject><subject>Exosomes - metabolism</subject><subject>Experiments</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Hirschsprung disease</subject><subject>Hirschsprung Disease - diagnosis</subject><subject>Hirschsprung Disease - genetics</subject><subject>Hirschsprung Disease - pathology</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Intercellular communication</subject><subject>Laboratories</subject><subject>Male</subject><subject>MicroRNAs</subject><subject>Microscopy</subject><subject>Mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - pathology</subject><subject>Nervous system</subject><subject>Neuronal development</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Original Research</subject><subject>Pediatrics</subject><subject>Peptides</subject><subject>Proteins - chemistry</subject><subject>Proteins - genetics</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Stem cells</subject><subject>Surgery</subject><subject>Toxicology</subject><issn>1178-2013</issn><issn>1176-9114</issn><issn>1178-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkt2LEzEUxYMo7lp98l0GfFCQqbn5mI8XoSxqK8sqqM8hk7lpU6aTMZkR_O_NbOu6FQkk4ebcX7iHQ8hzoEsGony7-XSz_AogKl49IJcAZZUzCvzhvfsFeRLjnlJZVkX9mFywspKcl_SSfFkNfhj96EzW4xR8n0c0AUdss_UNsMz1O9e4MWYGuy7Tt-LoYqpnaxei2cUhTP32VcxaF1FHfEoeWd1FfHY6F-T7h_ffrtb59eePm6vVdW4Eo2NeFKyRwNoCmK15U1gGFS2p1lpq3pqyEg2nWEtBmdWFRU2xaQxtobVYMyn4gmyO3NbrvRqCO-jwS3nt1G3Bh63SIY3VoWqAFpA2sMgEM6Y2tKxrwWVlS255lVjvjqxhag7YGuzHoLsz6PlL73Zq638qmciMQwK8PgGC_zFhHNXBxdkx3aOfooJKAHAxu74gL_-R7v0U-mSVYkxQoFwy8Ve11WkA11uf_jUzVK0kLYr0sZhVy_-o0mrx4Izv0bpUP2t4c2wwwccY0N7NCFTNYVIpTOoUpqR-cd-WO-2f9PDfaNXCPg</recordid><startdate>2016</startdate><enddate>2016</enddate><creator>Du, Chunxia</creator><creator>Xie, Hua</creator><creator>Zang, Rujin</creator><creator>Shen, Ziyang</creator><creator>Li, Hongxing</creator><creator>Chen, Pingfa</creator><creator>Xu, Xiaoqun</creator><creator>Xia, Yankai</creator><creator>Tang, Weibing</creator><general>Dove Medical Press Limited</general><general>Taylor & Francis Ltd</general><general>Dove Medical Press</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2016</creationdate><title>Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease</title><author>Du, Chunxia ; Xie, Hua ; Zang, Rujin ; Shen, Ziyang ; Li, Hongxing ; Chen, Pingfa ; Xu, Xiaoqun ; Xia, Yankai ; Tang, Weibing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-662b512d612f93b6f218070aaa5a3dc784b30e95402fa6fea0ebbc0d1dfe92543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Alzheimer's disease</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biomarkers - metabolism</topic><topic>Cancer</topic><topic>Case-Control Studies</topic><topic>Cell adhesion & migration</topic><topic>Cell Line</topic><topic>Colon - pathology</topic><topic>Congenital diseases</topic><topic>Cytochrome c</topic><topic>Cytochromes c - metabolism</topic><topic>Exosomal long non-coding RNA</topic><topic>Exosomes - metabolism</topic><topic>Experiments</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Hirschsprung disease</topic><topic>Hirschsprung Disease - diagnosis</topic><topic>Hirschsprung Disease - genetics</topic><topic>Hirschsprung Disease - pathology</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Intercellular communication</topic><topic>Laboratories</topic><topic>Male</topic><topic>MicroRNAs</topic><topic>Microscopy</topic><topic>Mitochondria</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - pathology</topic><topic>Nervous system</topic><topic>Neuronal development</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Original Research</topic><topic>Pediatrics</topic><topic>Peptides</topic><topic>Proteins - chemistry</topic><topic>Proteins - genetics</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Stem cells</topic><topic>Surgery</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Du, Chunxia</creatorcontrib><creatorcontrib>Xie, Hua</creatorcontrib><creatorcontrib>Zang, Rujin</creatorcontrib><creatorcontrib>Shen, Ziyang</creatorcontrib><creatorcontrib>Li, Hongxing</creatorcontrib><creatorcontrib>Chen, Pingfa</creatorcontrib><creatorcontrib>Xu, Xiaoqun</creatorcontrib><creatorcontrib>Xia, Yankai</creatorcontrib><creatorcontrib>Tang, Weibing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of nanomedicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Chunxia</au><au>Xie, Hua</au><au>Zang, Rujin</au><au>Shen, Ziyang</au><au>Li, Hongxing</au><au>Chen, Pingfa</au><au>Xu, Xiaoqun</au><au>Xia, Yankai</au><au>Tang, Weibing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease</atitle><jtitle>International journal of nanomedicine</jtitle><addtitle>Int J Nanomedicine</addtitle><date>2016</date><risdate>2016</risdate><volume>11</volume><spage>5871</spage><epage>5881</epage><pages>5871-5881</pages><issn>1178-2013</issn><issn>1176-9114</issn><eissn>1178-2013</eissn><abstract>Perturbation in apoptosis can lead to Hirschsprung's disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>27853370</pmid><doi>10.2147/IJN.S114838</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenosine Triphosphate - metabolism Alzheimer's disease Apoptosis Apoptosis - genetics Biomarkers - metabolism Cancer Case-Control Studies Cell adhesion & migration Cell Line Colon - pathology Congenital diseases Cytochrome c Cytochromes c - metabolism Exosomal long non-coding RNA Exosomes - metabolism Experiments Female Gene Expression Regulation Hirschsprung disease Hirschsprung Disease - diagnosis Hirschsprung Disease - genetics Hirschsprung Disease - pathology Humans Infant, Newborn Intercellular communication Laboratories Male MicroRNAs Microscopy Mitochondria Mitochondria - genetics Mitochondria - pathology Nervous system Neuronal development Neurons Neurons - metabolism Neurons - pathology Original Research Pediatrics Peptides Proteins - chemistry Proteins - genetics RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Stem cells Surgery Toxicology |
title | Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease |
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