Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP
Circular RNAs (circRNAs) are expressed at high levels in the brain and are involved in various CNS diseases. However, the potential role of circRNAs in ischemic stroke-associated neuronal injury remains largely unknown. Here, we investigated the important functions of circRNA (circTLK1) in this proc...
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| creator | Wu, Fangfang Han, Bing Wu, Shusheng Yang, Li Leng, Shuo Li, Mingyue Liao, Jiefeng Wang, Guangtian Ye, Qingqing Zhang, Yuan Chen, Haifeng Chen, Xufeng Zhong, Ming Xu, Yun Liu, Qiang Zhang, John H Yao, Honghong |
| description | Circular RNAs (circRNAs) are expressed at high levels in the brain and are involved in various CNS diseases. However, the potential role of circRNAs in ischemic stroke-associated neuronal injury remains largely unknown. Here, we investigated the important functions of circRNA
(circTLK1) in this process. The levels of circTLK1 were significantly increased in brain tissues in a mouse model of focal cerebral ischemia and reperfusion. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved neurological deficits. Furthermore, circTLK1 functioned as an endogenous miR-335-3p sponge to inhibit miR-335-3p activity, resulting in the increase of 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible poly (ADP-ribose) polymerase expression and a subsequent exacerbation of neuronal injury. Clinical studies confirmed increased levels of circTLK1 in the plasma of patients with acute ischemic stroke (59 males and 12 females). Our findings reveal a detrimental role of circTLK1 in ischemic brain injury.
The extent of neuronal injury after brain ischemia is a primary factor determining stroke outcomes. However, the molecular switches that control the death of ischemic neurons are poorly understood. While our previous studies indicated the involvement of circRNAs in ischemic stroke, the potential role of circRNAs in neuronal injury remains largely unknown. The levels of circTLK1 were significantly increased in the brain tissue and plasma isolated from animal models of ischemic stroke and patients. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved subsequent long-term neurological deficits. To our knowledge, these results provide the first definitive evidence that circTLK1 is detrimental in ischemic stroke. |
| doi_str_mv | 10.1523/JNEUROSCI.0299-19.2019 |
| format | Article |
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(circTLK1) in this process. The levels of circTLK1 were significantly increased in brain tissues in a mouse model of focal cerebral ischemia and reperfusion. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved neurological deficits. Furthermore, circTLK1 functioned as an endogenous miR-335-3p sponge to inhibit miR-335-3p activity, resulting in the increase of 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible poly (ADP-ribose) polymerase expression and a subsequent exacerbation of neuronal injury. Clinical studies confirmed increased levels of circTLK1 in the plasma of patients with acute ischemic stroke (59 males and 12 females). Our findings reveal a detrimental role of circTLK1 in ischemic brain injury.
The extent of neuronal injury after brain ischemia is a primary factor determining stroke outcomes. However, the molecular switches that control the death of ischemic neurons are poorly understood. While our previous studies indicated the involvement of circRNAs in ischemic stroke, the potential role of circRNAs in neuronal injury remains largely unknown. The levels of circTLK1 were significantly increased in the brain tissue and plasma isolated from animal models of ischemic stroke and patients. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved subsequent long-term neurological deficits. To our knowledge, these results provide the first definitive evidence that circTLK1 is detrimental in ischemic stroke.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.0299-19.2019</identifier><identifier>PMID: 31311824</identifier><language>eng</language><publisher>United States: Society for Neuroscience</publisher><subject>Adenosine diphosphate ; Aged ; Animals ; Brain ; Brain injury ; Brain Ischemia - diagnostic imaging ; Brain Ischemia - genetics ; Brain Ischemia - metabolism ; Circular RNA ; Dioxins ; Female ; Females ; Gene Knockdown Techniques - methods ; Head injuries ; Humans ; Ischemia ; Male ; Males ; Mice ; Mice, Inbred C57BL ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; Neurological diseases ; Neurons - metabolism ; Neurons - pathology ; Poly(ADP-ribose) Polymerases - genetics ; Poly(ADP-ribose) Polymerases - metabolism ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Reperfusion ; Ribonucleic acid ; Ribose ; RNA ; RNA, Circular - antagonists & inhibitors ; RNA, Circular - genetics ; RNA, Circular - metabolism ; Stroke ; Stroke - diagnostic imaging ; Stroke - genetics ; Stroke - metabolism</subject><ispartof>The Journal of neuroscience, 2019-09, Vol.39 (37), p.7369-7393</ispartof><rights>Copyright © 2019 the authors.</rights><rights>Copyright Society for Neuroscience Sep 11, 2019</rights><rights>Copyright © 2019 the authors 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-4319-4285</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6759031/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6759031/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31311824$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Fangfang</creatorcontrib><creatorcontrib>Han, Bing</creatorcontrib><creatorcontrib>Wu, Shusheng</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Leng, Shuo</creatorcontrib><creatorcontrib>Li, Mingyue</creatorcontrib><creatorcontrib>Liao, Jiefeng</creatorcontrib><creatorcontrib>Wang, Guangtian</creatorcontrib><creatorcontrib>Ye, Qingqing</creatorcontrib><creatorcontrib>Zhang, Yuan</creatorcontrib><creatorcontrib>Chen, Haifeng</creatorcontrib><creatorcontrib>Chen, Xufeng</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><creatorcontrib>Liu, Qiang</creatorcontrib><creatorcontrib>Zhang, John H</creatorcontrib><creatorcontrib>Yao, Honghong</creatorcontrib><title>Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Circular RNAs (circRNAs) are expressed at high levels in the brain and are involved in various CNS diseases. However, the potential role of circRNAs in ischemic stroke-associated neuronal injury remains largely unknown. Here, we investigated the important functions of circRNA
(circTLK1) in this process. The levels of circTLK1 were significantly increased in brain tissues in a mouse model of focal cerebral ischemia and reperfusion. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved neurological deficits. Furthermore, circTLK1 functioned as an endogenous miR-335-3p sponge to inhibit miR-335-3p activity, resulting in the increase of 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible poly (ADP-ribose) polymerase expression and a subsequent exacerbation of neuronal injury. Clinical studies confirmed increased levels of circTLK1 in the plasma of patients with acute ischemic stroke (59 males and 12 females). Our findings reveal a detrimental role of circTLK1 in ischemic brain injury.
The extent of neuronal injury after brain ischemia is a primary factor determining stroke outcomes. However, the molecular switches that control the death of ischemic neurons are poorly understood. While our previous studies indicated the involvement of circRNAs in ischemic stroke, the potential role of circRNAs in neuronal injury remains largely unknown. The levels of circTLK1 were significantly increased in the brain tissue and plasma isolated from animal models of ischemic stroke and patients. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved subsequent long-term neurological deficits. To our knowledge, these results provide the first definitive evidence that circTLK1 is detrimental in ischemic stroke.</description><subject>Adenosine diphosphate</subject><subject>Aged</subject><subject>Animals</subject><subject>Brain</subject><subject>Brain injury</subject><subject>Brain Ischemia - diagnostic imaging</subject><subject>Brain Ischemia - genetics</subject><subject>Brain Ischemia - metabolism</subject><subject>Circular RNA</subject><subject>Dioxins</subject><subject>Female</subject><subject>Females</subject><subject>Gene Knockdown Techniques - methods</subject><subject>Head injuries</subject><subject>Humans</subject><subject>Ischemia</subject><subject>Male</subject><subject>Males</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>Neurological diseases</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Poly(ADP-ribose) Polymerases - genetics</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Reperfusion</subject><subject>Ribonucleic acid</subject><subject>Ribose</subject><subject>RNA</subject><subject>RNA, Circular - antagonists & inhibitors</subject><subject>RNA, Circular - genetics</subject><subject>RNA, Circular - metabolism</subject><subject>Stroke</subject><subject>Stroke - diagnostic imaging</subject><subject>Stroke - genetics</subject><subject>Stroke - metabolism</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkFtLw0AUhBdRbK3-BVnwOXUvyW72RSj1Fi2txPocTpJNujWXukkK_nsXrKJP5zAzzMCH0CUlUxowfv20vHuLV6_zaEqYUh5VU0aoOkJj5yqP-YQeozFhknjCl_4InXXdlhAiCZWnaMQppzRk_hjZubHZUIHF8XKG14tnimdlaWEPve7wUg-2baDCUbMd7CeGJv_WqrY0mdNvdWEy03cYil5bHHXZRtcmw6-9bd813hvAtYk9zgOP767X0cssfjlHJwVUnb443Al6u79bzx-9xeohms8W3o4J2ntpkWuAMBRBSlL3KApcFoUSIhCZZj74vuR5zkKWSpG7GLAcQiaFUpoHLjxBN9-9uyGtdZ7pprdQJTtrarCfSQsm-e80ZpOU7T4RMlDEIZqgq0OBbT8G3fXJth2sw9EljCk3zwImXOry78xv_w9j_gVDk3_L</recordid><startdate>20190911</startdate><enddate>20190911</enddate><creator>Wu, Fangfang</creator><creator>Han, Bing</creator><creator>Wu, Shusheng</creator><creator>Yang, Li</creator><creator>Leng, Shuo</creator><creator>Li, Mingyue</creator><creator>Liao, Jiefeng</creator><creator>Wang, Guangtian</creator><creator>Ye, Qingqing</creator><creator>Zhang, Yuan</creator><creator>Chen, Haifeng</creator><creator>Chen, Xufeng</creator><creator>Zhong, Ming</creator><creator>Xu, Yun</creator><creator>Liu, Qiang</creator><creator>Zhang, John H</creator><creator>Yao, Honghong</creator><general>Society for Neuroscience</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QG</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4319-4285</orcidid></search><sort><creationdate>20190911</creationdate><title>Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP</title><author>Wu, Fangfang ; Han, Bing ; Wu, Shusheng ; Yang, Li ; Leng, Shuo ; Li, Mingyue ; Liao, Jiefeng ; Wang, Guangtian ; Ye, Qingqing ; Zhang, Yuan ; Chen, Haifeng ; Chen, Xufeng ; Zhong, Ming ; Xu, Yun ; Liu, Qiang ; Zhang, John H ; Yao, Honghong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p261t-bfdeaa8865b0baa891a37ff96656ce24a4473dd282b76d865a2da827699e351a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenosine diphosphate</topic><topic>Aged</topic><topic>Animals</topic><topic>Brain</topic><topic>Brain injury</topic><topic>Brain Ischemia - diagnostic imaging</topic><topic>Brain Ischemia - genetics</topic><topic>Brain Ischemia - metabolism</topic><topic>Circular RNA</topic><topic>Dioxins</topic><topic>Female</topic><topic>Females</topic><topic>Gene Knockdown Techniques - methods</topic><topic>Head injuries</topic><topic>Humans</topic><topic>Ischemia</topic><topic>Male</topic><topic>Males</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>Neurological diseases</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Poly(ADP-ribose) Polymerases - genetics</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Reperfusion</topic><topic>Ribonucleic acid</topic><topic>Ribose</topic><topic>RNA</topic><topic>RNA, Circular - antagonists & inhibitors</topic><topic>RNA, Circular - genetics</topic><topic>RNA, Circular - metabolism</topic><topic>Stroke</topic><topic>Stroke - diagnostic imaging</topic><topic>Stroke - genetics</topic><topic>Stroke - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Fangfang</creatorcontrib><creatorcontrib>Han, Bing</creatorcontrib><creatorcontrib>Wu, Shusheng</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Leng, Shuo</creatorcontrib><creatorcontrib>Li, Mingyue</creatorcontrib><creatorcontrib>Liao, Jiefeng</creatorcontrib><creatorcontrib>Wang, Guangtian</creatorcontrib><creatorcontrib>Ye, Qingqing</creatorcontrib><creatorcontrib>Zhang, Yuan</creatorcontrib><creatorcontrib>Chen, Haifeng</creatorcontrib><creatorcontrib>Chen, Xufeng</creatorcontrib><creatorcontrib>Zhong, Ming</creatorcontrib><creatorcontrib>Xu, Yun</creatorcontrib><creatorcontrib>Liu, Qiang</creatorcontrib><creatorcontrib>Zhang, John H</creatorcontrib><creatorcontrib>Yao, Honghong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Fangfang</au><au>Han, Bing</au><au>Wu, Shusheng</au><au>Yang, Li</au><au>Leng, Shuo</au><au>Li, Mingyue</au><au>Liao, Jiefeng</au><au>Wang, Guangtian</au><au>Ye, Qingqing</au><au>Zhang, Yuan</au><au>Chen, Haifeng</au><au>Chen, Xufeng</au><au>Zhong, Ming</au><au>Xu, Yun</au><au>Liu, Qiang</au><au>Zhang, John H</au><au>Yao, Honghong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2019-09-11</date><risdate>2019</risdate><volume>39</volume><issue>37</issue><spage>7369</spage><epage>7393</epage><pages>7369-7393</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>Circular RNAs (circRNAs) are expressed at high levels in the brain and are involved in various CNS diseases. However, the potential role of circRNAs in ischemic stroke-associated neuronal injury remains largely unknown. Here, we investigated the important functions of circRNA
(circTLK1) in this process. The levels of circTLK1 were significantly increased in brain tissues in a mouse model of focal cerebral ischemia and reperfusion. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved neurological deficits. Furthermore, circTLK1 functioned as an endogenous miR-335-3p sponge to inhibit miR-335-3p activity, resulting in the increase of 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible poly (ADP-ribose) polymerase expression and a subsequent exacerbation of neuronal injury. Clinical studies confirmed increased levels of circTLK1 in the plasma of patients with acute ischemic stroke (59 males and 12 females). Our findings reveal a detrimental role of circTLK1 in ischemic brain injury.
The extent of neuronal injury after brain ischemia is a primary factor determining stroke outcomes. However, the molecular switches that control the death of ischemic neurons are poorly understood. While our previous studies indicated the involvement of circRNAs in ischemic stroke, the potential role of circRNAs in neuronal injury remains largely unknown. The levels of circTLK1 were significantly increased in the brain tissue and plasma isolated from animal models of ischemic stroke and patients. Knockdown of circTLK1 significantly decreased infarct volumes, attenuated neuronal injury, and improved subsequent long-term neurological deficits. To our knowledge, these results provide the first definitive evidence that circTLK1 is detrimental in ischemic stroke.</abstract><cop>United States</cop><pub>Society for Neuroscience</pub><pmid>31311824</pmid><doi>10.1523/JNEUROSCI.0299-19.2019</doi><tpages>25</tpages><orcidid>https://orcid.org/0000-0002-4319-4285</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of neuroscience, 2019-09, Vol.39 (37), p.7369-7393 |
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| subjects | Adenosine diphosphate Aged Animals Brain Brain injury Brain Ischemia - diagnostic imaging Brain Ischemia - genetics Brain Ischemia - metabolism Circular RNA Dioxins Female Females Gene Knockdown Techniques - methods Head injuries Humans Ischemia Male Males Mice Mice, Inbred C57BL MicroRNAs - genetics MicroRNAs - metabolism Middle Aged Neurological diseases Neurons - metabolism Neurons - pathology Poly(ADP-ribose) Polymerases - genetics Poly(ADP-ribose) Polymerases - metabolism Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Reperfusion Ribonucleic acid Ribose RNA RNA, Circular - antagonists & inhibitors RNA, Circular - genetics RNA, Circular - metabolism Stroke Stroke - diagnostic imaging Stroke - genetics Stroke - metabolism |
| title | Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP |
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