Disrupted in Schizophrenia 1 Reverse Ectopic Migration of Neural Precursors in Mouse Hilus After Pilocarpine-Induced Status Epilepticus
Neural precursors in the subgranular zone (SGZ) can be stimulated by status epilepticus (SE) and ectopically migrate to the hilus. These mislocated cells serve as “potential pacemakers” of spontaneous recurrent seizures, and targeting them could potentially reverse the seizure process. Disrupted-in-...
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description | Neural precursors in the subgranular zone (SGZ) can be stimulated by status epilepticus (SE) and ectopically migrate to the hilus. These mislocated cells serve as “potential pacemakers” of spontaneous recurrent seizures, and targeting them could potentially reverse the seizure process. Disrupted-in-Schizophrenia 1 (DISC1) regulates hippocampal neurogenesis after seizures both in vitro and in vivo. Our previous study found that DISC1 was colocalized with neural precursors in the hilus after SE. However, its molecular mechanism and pathways contribute to the ectopic migration of neural precursors to the hilus induced by SE awaits exploration. Here, we showed that both Reelin-ApoER2/EphB2 and Reelin-Integrin β1/Integrin α5 axes may participate in the modulation of neurogenesis after SE. Especially, DISC1, as a protective role, might partly reversed the ectopic progenitor migration via EphB2 pathway. Our findings demonstrated that DISC1 played a protective role in the ectopic migration of neural precursors induced by SE insults and DISC1 could be an attractive new target for the treatment of epilepsy. |
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These mislocated cells serve as “potential pacemakers” of spontaneous recurrent seizures, and targeting them could potentially reverse the seizure process. Disrupted-in-Schizophrenia 1 (DISC1) regulates hippocampal neurogenesis after seizures both in vitro and in vivo. Our previous study found that DISC1 was colocalized with neural precursors in the hilus after SE. However, its molecular mechanism and pathways contribute to the ectopic migration of neural precursors to the hilus induced by SE awaits exploration. Here, we showed that both Reelin-ApoER2/EphB2 and Reelin-Integrin β1/Integrin α5 axes may participate in the modulation of neurogenesis after SE. Especially, DISC1, as a protective role, might partly reversed the ectopic progenitor migration via EphB2 pathway. 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Our findings demonstrated that DISC1 played a protective role in the ectopic migration of neural precursors induced by SE insults and DISC1 could be an attractive new target for the treatment of epilepsy.</description><subject>Apolipoprotein E</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Convulsions & seizures</subject><subject>Disc1 protein</subject><subject>Epilepsy</subject><subject>Hippocampus</subject><subject>Mental disorders</subject><subject>Molecular modelling</subject><subject>Neural stem cells</subject><subject>Neurobiology</subject><subject>Neurogenesis</subject><subject>Neurology</subject><subject>Neuromodulation</subject><subject>Neurosciences</subject><subject>Pilocarpine</subject><subject>Reelin protein</subject><subject>Schizophrenia</subject><subject>Seizures</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kUFPFDEUgBujkRX9Ax5MEy9eqn3tdNs5EliEBJSInifdziuUzE7HdmoCf4C_TZdFTTx4eod-_d5LPkLeAv8InOtPGQSXinEhWZ1cs-YZWYBSLQMw4jlZcNNKppeN2SOvcr7hXAjg-iXZk7rRrVGwIPdHIacyzdjTMNJLdx3u4nSdcAyWAv2GvzBlpCs3xyk4eh6ukp1DHGn09AuWZAd6kdCVlGPKW8N5LJU_CUPJ9MDPmOhFGKKzaQojstOxL66uupztXIHVFAac5uBKfk1eeDtkfPM098mP49X3wxN29vXz6eHBGXNS85mhQrtuAZbOg7LCOtUIK7zTPYL2a-ilNxzXzrSmtSgN6t4svQIpVaPAKrlPPuy8U4o_C-a524TscBjsiPX0TpgGuADFm4q-_we9iSWN9bpKLVvZctPoSokd5VLMOaHvphQ2Nt12wLttpm6XqauZusdM3Vb97kld1hvs_3z53aUCcgfk-jReYfq7-z_aBw6Jnwg</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Chen, Lu</creator><creator>Xu, Jing</creator><creator>Zhu, Lin</creator><creator>Xu, Puying</creator><creator>Chang, Lvhua</creator><creator>Han, Yanbing</creator><creator>Wu, Qian</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6259-7434</orcidid></search><sort><creationdate>20231101</creationdate><title>Disrupted in Schizophrenia 1 Reverse Ectopic Migration of Neural Precursors in Mouse Hilus After Pilocarpine-Induced Status Epilepticus</title><author>Chen, Lu ; Xu, Jing ; Zhu, Lin ; Xu, Puying ; Chang, Lvhua ; Han, Yanbing ; Wu, Qian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-e5eab9116cf15a2ac542a2fc7de17fb1d3f80ebc8989ae38e7d86f51335451a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apolipoprotein E</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Convulsions & seizures</topic><topic>Disc1 protein</topic><topic>Epilepsy</topic><topic>Hippocampus</topic><topic>Mental disorders</topic><topic>Molecular modelling</topic><topic>Neural stem cells</topic><topic>Neurobiology</topic><topic>Neurogenesis</topic><topic>Neurology</topic><topic>Neuromodulation</topic><topic>Neurosciences</topic><topic>Pilocarpine</topic><topic>Reelin protein</topic><topic>Schizophrenia</topic><topic>Seizures</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Lu</creatorcontrib><creatorcontrib>Xu, Jing</creatorcontrib><creatorcontrib>Zhu, Lin</creatorcontrib><creatorcontrib>Xu, Puying</creatorcontrib><creatorcontrib>Chang, Lvhua</creatorcontrib><creatorcontrib>Han, Yanbing</creatorcontrib><creatorcontrib>Wu, Qian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Lu</au><au>Xu, Jing</au><au>Zhu, Lin</au><au>Xu, Puying</au><au>Chang, Lvhua</au><au>Han, Yanbing</au><au>Wu, Qian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disrupted in Schizophrenia 1 Reverse Ectopic Migration of Neural Precursors in Mouse Hilus After Pilocarpine-Induced Status Epilepticus</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2023-11-01</date><risdate>2023</risdate><volume>60</volume><issue>11</issue><spage>6689</spage><epage>6703</epage><pages>6689-6703</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Neural precursors in the subgranular zone (SGZ) can be stimulated by status epilepticus (SE) and ectopically migrate to the hilus. These mislocated cells serve as “potential pacemakers” of spontaneous recurrent seizures, and targeting them could potentially reverse the seizure process. Disrupted-in-Schizophrenia 1 (DISC1) regulates hippocampal neurogenesis after seizures both in vitro and in vivo. Our previous study found that DISC1 was colocalized with neural precursors in the hilus after SE. However, its molecular mechanism and pathways contribute to the ectopic migration of neural precursors to the hilus induced by SE awaits exploration. Here, we showed that both Reelin-ApoER2/EphB2 and Reelin-Integrin β1/Integrin α5 axes may participate in the modulation of neurogenesis after SE. Especially, DISC1, as a protective role, might partly reversed the ectopic progenitor migration via EphB2 pathway. Our findings demonstrated that DISC1 played a protective role in the ectopic migration of neural precursors induced by SE insults and DISC1 could be an attractive new target for the treatment of epilepsy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37479851</pmid><doi>10.1007/s12035-023-03507-4</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-6259-7434</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Apolipoprotein E Biomedical and Life Sciences Biomedicine Cell Biology Convulsions & seizures Disc1 protein Epilepsy Hippocampus Mental disorders Molecular modelling Neural stem cells Neurobiology Neurogenesis Neurology Neuromodulation Neurosciences Pilocarpine Reelin protein Schizophrenia Seizures |
title | Disrupted in Schizophrenia 1 Reverse Ectopic Migration of Neural Precursors in Mouse Hilus After Pilocarpine-Induced Status Epilepticus |
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