microRNA-124 targets glucocorticoid receptor and is involved in depression-like behaviors
Dysregulation of microRNA (miRNA) has been shown to be involved in early observations of depression. MicroRNA-124-3p (miR-124) is the most abundant microRNA in the brain. Previous studies have shown that miR-124 plays a major role in depression. Here we showed that miR-124 directly targeted glucocor...
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Veröffentlicht in: | Progress in neuro-psychopharmacology & biological psychiatry 2017-10, Vol.79 (Pt B), p.417-425 |
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description | Dysregulation of microRNA (miRNA) has been shown to be involved in early observations of depression. MicroRNA-124-3p (miR-124) is the most abundant microRNA in the brain. Previous studies have shown that miR-124 plays a major role in depression. Here we showed that miR-124 directly targeted glucocorticoid receptor (GR) in HEK 293 cells. In addition, inhibition of miR-124 by its antagomir (2nmol/every two days) could reverse the decrease of sucrose preference and the increase of immobility time in mice exposed to chronic corticosterone (CORT, 40mg/kg) injection. Moreover, these effects on behavioral improvement were coupled to the activation of brain-derived neurotrophic factor (BDNF), TrkB, ERK, and CREB, as well as the induction of synaptogenesis and neuronal proliferation. Altogether, our study suggests that miR-124 can be served as a biomarker for depression and a novel target for drug development, and demonstrates that inhibition of miR-124 may be a strategy for treating depression by activating BDNF-TrkB signaling pathway in the hippocampus.
•miR-124 antagomir produced antidepressant in corticosterone-induced depression.•GR and BDNF up-regulation engaged during the antidepressant of miR-124 antagomir.•miR-124 can directly target GR. |
doi_str_mv | 10.1016/j.pnpbp.2017.07.024 |
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•miR-124 antagomir produced antidepressant in corticosterone-induced depression.•GR and BDNF up-regulation engaged during the antidepressant of miR-124 antagomir.•miR-124 can directly target GR.</description><identifier>ISSN: 0278-5846</identifier><identifier>EISSN: 1878-4216</identifier><identifier>DOI: 10.1016/j.pnpbp.2017.07.024</identifier><identifier>PMID: 28764913</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Animals ; Antagomirs - pharmacology ; Antidepressive Agents - pharmacology ; Brain-derived neurotrophic factor (BDNF) ; Brain-Derived Neurotrophic Factor - metabolism ; Corticosterone ; Depression ; Depressive Disorder - drug therapy ; Depressive Disorder - metabolism ; Depressive Disorder - pathology ; Disease Models, Animal ; Glucocorticoid receptor (GR) ; HEK293 Cells ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Humans ; Male ; Mice, Inbred C57BL ; microRNA (miRNA) ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - metabolism ; Neurons - drug effects ; Neurons - metabolism ; Neurons - pathology ; Protein Interaction Domains and Motifs ; Random Allocation ; Receptors, Glucocorticoid - genetics ; Receptors, Glucocorticoid - metabolism ; RNA, Messenger - metabolism</subject><ispartof>Progress in neuro-psychopharmacology & biological psychiatry, 2017-10, Vol.79 (Pt B), p.417-425</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-54c1681a086df2d8d171569b25e4f0523e0124e2bfe98b3e7c732126f5d42d763</citedby><cites>FETCH-LOGICAL-c359t-54c1681a086df2d8d171569b25e4f0523e0124e2bfe98b3e7c732126f5d42d763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.pnpbp.2017.07.024$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28764913$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Shuang-Shuang</creatorcontrib><creatorcontrib>Mu, Rong-Hao</creatorcontrib><creatorcontrib>Li, Cheng-Fu</creatorcontrib><creatorcontrib>Dong, Shu-Qi</creatorcontrib><creatorcontrib>Geng, Di</creatorcontrib><creatorcontrib>Liu, Qing</creatorcontrib><creatorcontrib>Yi, Li-Tao</creatorcontrib><title>microRNA-124 targets glucocorticoid receptor and is involved in depression-like behaviors</title><title>Progress in neuro-psychopharmacology & biological psychiatry</title><addtitle>Prog Neuropsychopharmacol Biol Psychiatry</addtitle><description>Dysregulation of microRNA (miRNA) has been shown to be involved in early observations of depression. MicroRNA-124-3p (miR-124) is the most abundant microRNA in the brain. Previous studies have shown that miR-124 plays a major role in depression. Here we showed that miR-124 directly targeted glucocorticoid receptor (GR) in HEK 293 cells. In addition, inhibition of miR-124 by its antagomir (2nmol/every two days) could reverse the decrease of sucrose preference and the increase of immobility time in mice exposed to chronic corticosterone (CORT, 40mg/kg) injection. Moreover, these effects on behavioral improvement were coupled to the activation of brain-derived neurotrophic factor (BDNF), TrkB, ERK, and CREB, as well as the induction of synaptogenesis and neuronal proliferation. Altogether, our study suggests that miR-124 can be served as a biomarker for depression and a novel target for drug development, and demonstrates that inhibition of miR-124 may be a strategy for treating depression by activating BDNF-TrkB signaling pathway in the hippocampus.
•miR-124 antagomir produced antidepressant in corticosterone-induced depression.•GR and BDNF up-regulation engaged during the antidepressant of miR-124 antagomir.•miR-124 can directly target GR.</description><subject>Animals</subject><subject>Antagomirs - pharmacology</subject><subject>Antidepressive Agents - pharmacology</subject><subject>Brain-derived neurotrophic factor (BDNF)</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Corticosterone</subject><subject>Depression</subject><subject>Depressive Disorder - drug therapy</subject><subject>Depressive Disorder - metabolism</subject><subject>Depressive Disorder - pathology</subject><subject>Disease Models, Animal</subject><subject>Glucocorticoid receptor (GR)</subject><subject>HEK293 Cells</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Humans</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>microRNA (miRNA)</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - metabolism</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Protein Interaction Domains and Motifs</subject><subject>Random Allocation</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>RNA, Messenger - metabolism</subject><issn>0278-5846</issn><issn>1878-4216</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9r3DAQxUVo6G62_QSB4GMv3mj0z_KhhxDaJrA0EJJDT8KWxqm2XsuV7IV--yjZTY6FgXmHN_NmfoScA10DBXW5XY_D2I5rRqFa01xMnJAl6EqXgoH6QJaUZS21UAtyltKWUgqc8o9kwXSlRA18SX7tvI3h_udVCUwUUxOfcErFUz_bYEOcvA3eFREtjlOIRTO4wqfCD_vQ7zHroXA4RkzJh6Hs_R8sWvzd7H2I6RM57Zo-4edjX5HH798erm_Kzd2P2-urTWm5rKdSCgtKQ0O1ch1z2kEFUtUtkyg6KhlHmi9D1nZY65ZjZSvOgKlOOsFcpfiKfDnsHWP4O2OazM4ni33fDBjmZKBmUgKAZtnKD9b8ckoROzNGv2viPwPUvDA1W_PK1LwwNTQXE3nq4hgwtzt07zNvELPh68GA-c29x2iS9ThYdD6Tm4wL_r8BzzOIiK4</recordid><startdate>20171003</startdate><enddate>20171003</enddate><creator>Wang, Shuang-Shuang</creator><creator>Mu, Rong-Hao</creator><creator>Li, Cheng-Fu</creator><creator>Dong, Shu-Qi</creator><creator>Geng, Di</creator><creator>Liu, Qing</creator><creator>Yi, Li-Tao</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20171003</creationdate><title>microRNA-124 targets glucocorticoid receptor and is involved in depression-like behaviors</title><author>Wang, Shuang-Shuang ; Mu, Rong-Hao ; Li, Cheng-Fu ; Dong, Shu-Qi ; Geng, Di ; Liu, Qing ; Yi, Li-Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-54c1681a086df2d8d171569b25e4f0523e0124e2bfe98b3e7c732126f5d42d763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antagomirs - pharmacology</topic><topic>Antidepressive Agents - pharmacology</topic><topic>Brain-derived neurotrophic factor (BDNF)</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Corticosterone</topic><topic>Depression</topic><topic>Depressive Disorder - drug therapy</topic><topic>Depressive Disorder - metabolism</topic><topic>Depressive Disorder - pathology</topic><topic>Disease Models, Animal</topic><topic>Glucocorticoid receptor (GR)</topic><topic>HEK293 Cells</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Humans</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>microRNA (miRNA)</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - metabolism</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Protein Interaction Domains and Motifs</topic><topic>Random Allocation</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Shuang-Shuang</creatorcontrib><creatorcontrib>Mu, Rong-Hao</creatorcontrib><creatorcontrib>Li, Cheng-Fu</creatorcontrib><creatorcontrib>Dong, Shu-Qi</creatorcontrib><creatorcontrib>Geng, Di</creatorcontrib><creatorcontrib>Liu, Qing</creatorcontrib><creatorcontrib>Yi, Li-Tao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Progress in neuro-psychopharmacology & biological psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Shuang-Shuang</au><au>Mu, Rong-Hao</au><au>Li, Cheng-Fu</au><au>Dong, Shu-Qi</au><au>Geng, Di</au><au>Liu, Qing</au><au>Yi, Li-Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA-124 targets glucocorticoid receptor and is involved in depression-like behaviors</atitle><jtitle>Progress in neuro-psychopharmacology & biological psychiatry</jtitle><addtitle>Prog Neuropsychopharmacol Biol Psychiatry</addtitle><date>2017-10-03</date><risdate>2017</risdate><volume>79</volume><issue>Pt B</issue><spage>417</spage><epage>425</epage><pages>417-425</pages><issn>0278-5846</issn><eissn>1878-4216</eissn><abstract>Dysregulation of microRNA (miRNA) has been shown to be involved in early observations of depression. MicroRNA-124-3p (miR-124) is the most abundant microRNA in the brain. Previous studies have shown that miR-124 plays a major role in depression. Here we showed that miR-124 directly targeted glucocorticoid receptor (GR) in HEK 293 cells. In addition, inhibition of miR-124 by its antagomir (2nmol/every two days) could reverse the decrease of sucrose preference and the increase of immobility time in mice exposed to chronic corticosterone (CORT, 40mg/kg) injection. Moreover, these effects on behavioral improvement were coupled to the activation of brain-derived neurotrophic factor (BDNF), TrkB, ERK, and CREB, as well as the induction of synaptogenesis and neuronal proliferation. Altogether, our study suggests that miR-124 can be served as a biomarker for depression and a novel target for drug development, and demonstrates that inhibition of miR-124 may be a strategy for treating depression by activating BDNF-TrkB signaling pathway in the hippocampus.
•miR-124 antagomir produced antidepressant in corticosterone-induced depression.•GR and BDNF up-regulation engaged during the antidepressant of miR-124 antagomir.•miR-124 can directly target GR.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>28764913</pmid><doi>10.1016/j.pnpbp.2017.07.024</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Antagomirs - pharmacology Antidepressive Agents - pharmacology Brain-derived neurotrophic factor (BDNF) Brain-Derived Neurotrophic Factor - metabolism Corticosterone Depression Depressive Disorder - drug therapy Depressive Disorder - metabolism Depressive Disorder - pathology Disease Models, Animal Glucocorticoid receptor (GR) HEK293 Cells Hippocampus Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Humans Male Mice, Inbred C57BL microRNA (miRNA) MicroRNAs - antagonists & inhibitors MicroRNAs - metabolism Neurons - drug effects Neurons - metabolism Neurons - pathology Protein Interaction Domains and Motifs Random Allocation Receptors, Glucocorticoid - genetics Receptors, Glucocorticoid - metabolism RNA, Messenger - metabolism |
title | microRNA-124 targets glucocorticoid receptor and is involved in depression-like behaviors |
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