<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang KL</submitter><funding>the Science and Technology Foundation in Guangdong Province</funding><funding>the Fundamental Research Funds for the Central Universities</funding><funding>the National Natural Science Foundation of Guangdong Province</funding><funding>National Natural Science Foundation of China</funding><funding>the Shenzhen Fundamental Research Program</funding><funding>the Science and Technology Foundation in Guangzhou City</funding><funding>the Futian District Health and Public Welfare Research Project of Shenzhen City</funding><pagination>2989-3003</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10333378</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(6)</volume><pubmed_abstract>Elabela (ELA), which is the second endogenous peptide ligand of the apelin receptor (APJ) to be discovered, has been widely studied for potential use as a therapeutic peptide. However, its role in ischemic stroke (IS), which is a leading cause of disability and death worldwide and has limited therapeutic options, is uncertain. The aim of the present study was to investigate the beneficial effects of ELA on neuron survival after ischemia and the underlying molecular mechanisms. Primary cortical neurons were isolated from the cerebral cortex of pregnant C57BL/6J mice. Flow cytometry and immunofluorescence showed that ELA inhibited oxygen-glucose deprivation (OGD) -induced apoptosis and axonal damage in vitro. Additionally, analysis of the Gene Expression Omnibus database revealed that the ex</pubmed_abstract><journal>Cellular and molecular neurobiology</journal><pubmed_title>Elabela, a Novel Peptide, Exerts Neuroprotective Effects Against Ischemic Stroke Through the APJ/miR-124-3p/CTDSP1/AKT Pathway.</pubmed_title><pmcid>PMC10333378</pmcid><funding_grant_id>No. 2017A030313503</funding_grant_id><funding_grant_id>No. FTWS2019001, FTWS2021016, FTWS2022018</funding_grant_id><funding_grant_id>No. 81070125, 81270213, 81670306</funding_grant_id><funding_grant_id>No. 13ykzd16, 17ykjc18</funding_grant_id><funding_grant_id>No. JCYJ20190808101405466, JCYJ20210324115003008, JCYJ20220530144404009</funding_grant_id><funding_grant_id>No. 201806020084</funding_grant_id><funding_grant_id>No. 2010B031600032, 2014A020211002</funding_grant_id><pubmed_authors>Zhang KL</pubmed_authors><pubmed_authors>Zhou CQ</pubmed_authors><pubmed_authors>Fu JY</pubmed_authors><pubmed_authors>Wu HD</pubmed_authors><pubmed_authors>Li SM</pubmed_authors><pubmed_authors>Hong YH</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Chen XX</pubmed_authors><pubmed_authors>Zheng GH</pubmed_authors><pubmed_authors>Zeng CT</pubmed_authors><pubmed_authors>Hou JY</pubmed_authors><pubmed_authors>Wu H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Elabela, a Novel Peptide, Exerts Neuroprotective Effects Against Ischemic Stroke Through the APJ/miR-124-3p/CTDSP1/AKT Pathway.</name><description>Elabela (ELA), which is the second endogenous peptide ligand of the apelin receptor (APJ) to be discovered, has been widely studied for potential use as a therapeutic peptide. However, its role in ischemic stroke (IS), which is a leading cause of disability and death worldwide and has limited therapeutic options, is uncertain. The aim of the present study was to investigate the beneficial effects of ELA on neuron survival after ischemia and the underlying molecular mechanisms. Primary cortical neurons were isolated from the cerebral cortex of pregnant C57BL/6J mice. Flow cytometry and immunofluorescence showed that ELA inhibited oxygen-glucose deprivation (OGD) -induced apoptosis and axonal damage in vitro. Additionally, analysis of the Gene Expression Omnibus database revealed that the ex</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Aug</publication><modification>2026-05-29T00:14:15.372Z</modification><creation>2025-04-04T20:29:22.407Z</creation></dates><accession>S-EPMC10333378</accession><cross_references><pubmed>37106272</pubmed><doi>10.1007/s10571-023-01352-6</doi></cross_references></HashMap>