microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes
Temporal lobe epilepsy (TLE) is a chronic neurological disease in humans, which is refractory to pharmacological treatment in about 30% of the patients. Reactive glial cells are thought to play a major role during the development of epilepsy (epileptogenesis) via regulation of brain inflammation and...
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| Veröffentlicht in: | Glia 2020-01, Vol.68 (1), p.60-75 |
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| creator | Korotkov, Anatoly Broekaart, Diede W. M. Banchaewa, Leyla Pustjens, Ben Scheppingen, Jackelien Anink, Jasper J. Baayen, Johannes C. Idema, Sander Gorter, Jan A. Vliet, Erwin A. Aronica, Eleonora |
| description | Temporal lobe epilepsy (TLE) is a chronic neurological disease in humans, which is refractory to pharmacological treatment in about 30% of the patients. Reactive glial cells are thought to play a major role during the development of epilepsy (epileptogenesis) via regulation of brain inflammation and remodeling of the extracellular matrix (ECM). These processes can be regulated by microRNAs (miRs), a class of small non‐coding RNAs, which can control entire gene networks at a post‐transcriptional level. The expression of miRs is known to change dynamically during epileptogenesis. miR‐132 is one of the most commonly upregulated miRs in animal TLE models with important roles shown in neurons. However, the possible role of miR‐132 in glia remains largely unknown. The aim of this study was to characterize the cell‐type specific expression of miR‐132 in the hippocampus of patients with TLE and during epileptogenesis in a rat TLE model. Furthermore, the potential role of miR‐132 was investigated by transfection of human primary cultured astrocytes that were stimulated with the cytokines IL‐1β or TGF‐β1. We showed an increased expression of miR‐132 in the human and rat epileptogenic hippocampus, particularly in glial cells. Transfection of miR‐132 in human primary astrocytes reduced the expression of pro‐epileptogenic COX‐2, IL‐1β, TGF‐β2, CCL2, and MMP3. This suggests that miR‐132, particularly in astrocytes, represents a potential therapeutic target that warrants further in vivo investigation.
Main Points
miR‐132 expression is increased in the epileptogenic human and rat hippocampus.
miR‐132 is expressed by reactive glia.
miR‐132 attenuates expression of pro-epileptogenic factors in cultured human astrocytes. |
| doi_str_mv | 10.1002/glia.23700 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6899748</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2272738532</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4480-d9e723d553c94a81e9aa6a3da18a7d7589b091b1b81a59c954d6b99a7e091f193</originalsourceid><addsrcrecordid>eNp9kc-KFDEQh4Mo7rh68QEk4EWEXlNJ_0kuwrDoujAoiJ5DOl09k6W70ybdq3PzETz6fD6JaXtd1IOnolJfPqr4EfIY2Bkwxl_sO2fOuKgYu0M2wJTMAER5l2yYVHkGuYIT8iDGK8YgNdV9ciIgZ5KLckO-984G__7t9sfXbyA4dZH6awz4ZQwYIzbUDXTxL3XCfvTBdLTzNVIcXYdjPFIzNDRgM1uMdDqkwfrX-YH6lo7BJ_UKT36Pg7O0NXbyIS7Ow9ybgdq5m-bkoCZOwdvjhPEhudeaLuKjm3pKPr5-9eH8TbZ7d3F5vt1lNs8lyxqFFRdNUQirciMBlTGlEY0BaaqmKqSqmYIaagmmUFYVeVPWSpkK03MLSpySl6t3nOseG4vDlE7UY3C9CUftjdN_TwZ30Ht_rUupVJXLJHh2Iwj-04xx0r2LFrvODOjnqDmveCVkIXhCn_6DXvk5DOk8zQUIJQEKkajnK5WCiTFge7sMML0ErpdA9K_AE_zkz_Vv0d8JJwBW4HNK4Pgflb7YXW5X6U9bQbsq</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2313981153</pqid></control><display><type>article</type><title>microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Korotkov, Anatoly ; Broekaart, Diede W. M. ; Banchaewa, Leyla ; Pustjens, Ben ; Scheppingen, Jackelien ; Anink, Jasper J. ; Baayen, Johannes C. ; Idema, Sander ; Gorter, Jan A. ; Vliet, Erwin A. ; Aronica, Eleonora</creator><creatorcontrib>Korotkov, Anatoly ; Broekaart, Diede W. M. ; Banchaewa, Leyla ; Pustjens, Ben ; Scheppingen, Jackelien ; Anink, Jasper J. ; Baayen, Johannes C. ; Idema, Sander ; Gorter, Jan A. ; Vliet, Erwin A. ; Aronica, Eleonora</creatorcontrib><description>Temporal lobe epilepsy (TLE) is a chronic neurological disease in humans, which is refractory to pharmacological treatment in about 30% of the patients. Reactive glial cells are thought to play a major role during the development of epilepsy (epileptogenesis) via regulation of brain inflammation and remodeling of the extracellular matrix (ECM). These processes can be regulated by microRNAs (miRs), a class of small non‐coding RNAs, which can control entire gene networks at a post‐transcriptional level. The expression of miRs is known to change dynamically during epileptogenesis. miR‐132 is one of the most commonly upregulated miRs in animal TLE models with important roles shown in neurons. However, the possible role of miR‐132 in glia remains largely unknown. The aim of this study was to characterize the cell‐type specific expression of miR‐132 in the hippocampus of patients with TLE and during epileptogenesis in a rat TLE model. Furthermore, the potential role of miR‐132 was investigated by transfection of human primary cultured astrocytes that were stimulated with the cytokines IL‐1β or TGF‐β1. We showed an increased expression of miR‐132 in the human and rat epileptogenic hippocampus, particularly in glial cells. Transfection of miR‐132 in human primary astrocytes reduced the expression of pro‐epileptogenic COX‐2, IL‐1β, TGF‐β2, CCL2, and MMP3. This suggests that miR‐132, particularly in astrocytes, represents a potential therapeutic target that warrants further in vivo investigation.
Main Points
miR‐132 expression is increased in the epileptogenic human and rat hippocampus.
miR‐132 is expressed by reactive glia.
miR‐132 attenuates expression of pro-epileptogenic factors in cultured human astrocytes.</description><identifier>ISSN: 0894-1491</identifier><identifier>EISSN: 1098-1136</identifier><identifier>DOI: 10.1002/glia.23700</identifier><identifier>PMID: 31408236</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Animal models ; Animals ; Astrocytes ; Astrocytes - metabolism ; Astrocytes - pathology ; Cells, Cultured ; Cytokines ; Drug therapy ; Epilepsy ; Epilepsy, Temporal Lobe - genetics ; Epilepsy, Temporal Lobe - metabolism ; Epilepsy, Temporal Lobe - pathology ; epileptogenesis ; Extracellular matrix ; Female ; Gene Expression ; Glial cells ; Hippocampus ; Hippocampus - metabolism ; Hippocampus - pathology ; Humans ; IL‐1 beta ; In vivo methods and tests ; Male ; MicroRNAs ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; Middle Aged ; miRNA ; Monocyte chemoattractant protein 1 ; Neuroglia - metabolism ; Neuroglia - pathology ; neuroinflammation ; Neurological diseases ; Neuronal-glial interactions ; Non-coding RNA ; Rats ; Rats, Sprague-Dawley ; Ribonucleic acid ; RNA ; Temporal lobe ; TGF‐beta ; Therapeutic applications ; Transcription ; Transfection ; Transforming growth factor-b1 ; Young Adult</subject><ispartof>Glia, 2020-01, Vol.68 (1), p.60-75</ispartof><rights>2019 The Authors. published by Wiley Periodicals, Inc.</rights><rights>2019 The Authors. Glia published by Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4480-d9e723d553c94a81e9aa6a3da18a7d7589b091b1b81a59c954d6b99a7e091f193</citedby><cites>FETCH-LOGICAL-c4480-d9e723d553c94a81e9aa6a3da18a7d7589b091b1b81a59c954d6b99a7e091f193</cites><orcidid>0000-0002-3542-3770 ; 0000-0002-0532-4798 ; 0000-0001-5747-3202 ; 0000-0002-8313-6282 ; 0000-0002-4842-0659 ; 0000-0003-3842-1700 ; 0000-0002-0671-857X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fglia.23700$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fglia.23700$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31408236$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Korotkov, Anatoly</creatorcontrib><creatorcontrib>Broekaart, Diede W. M.</creatorcontrib><creatorcontrib>Banchaewa, Leyla</creatorcontrib><creatorcontrib>Pustjens, Ben</creatorcontrib><creatorcontrib>Scheppingen, Jackelien</creatorcontrib><creatorcontrib>Anink, Jasper J.</creatorcontrib><creatorcontrib>Baayen, Johannes C.</creatorcontrib><creatorcontrib>Idema, Sander</creatorcontrib><creatorcontrib>Gorter, Jan A.</creatorcontrib><creatorcontrib>Vliet, Erwin A.</creatorcontrib><creatorcontrib>Aronica, Eleonora</creatorcontrib><title>microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes</title><title>Glia</title><addtitle>Glia</addtitle><description>Temporal lobe epilepsy (TLE) is a chronic neurological disease in humans, which is refractory to pharmacological treatment in about 30% of the patients. Reactive glial cells are thought to play a major role during the development of epilepsy (epileptogenesis) via regulation of brain inflammation and remodeling of the extracellular matrix (ECM). These processes can be regulated by microRNAs (miRs), a class of small non‐coding RNAs, which can control entire gene networks at a post‐transcriptional level. The expression of miRs is known to change dynamically during epileptogenesis. miR‐132 is one of the most commonly upregulated miRs in animal TLE models with important roles shown in neurons. However, the possible role of miR‐132 in glia remains largely unknown. The aim of this study was to characterize the cell‐type specific expression of miR‐132 in the hippocampus of patients with TLE and during epileptogenesis in a rat TLE model. Furthermore, the potential role of miR‐132 was investigated by transfection of human primary cultured astrocytes that were stimulated with the cytokines IL‐1β or TGF‐β1. We showed an increased expression of miR‐132 in the human and rat epileptogenic hippocampus, particularly in glial cells. Transfection of miR‐132 in human primary astrocytes reduced the expression of pro‐epileptogenic COX‐2, IL‐1β, TGF‐β2, CCL2, and MMP3. This suggests that miR‐132, particularly in astrocytes, represents a potential therapeutic target that warrants further in vivo investigation.
Main Points
miR‐132 expression is increased in the epileptogenic human and rat hippocampus.
miR‐132 is expressed by reactive glia.
miR‐132 attenuates expression of pro-epileptogenic factors in cultured human astrocytes.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animal models</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - pathology</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Drug therapy</subject><subject>Epilepsy</subject><subject>Epilepsy, Temporal Lobe - genetics</subject><subject>Epilepsy, Temporal Lobe - metabolism</subject><subject>Epilepsy, Temporal Lobe - pathology</subject><subject>epileptogenesis</subject><subject>Extracellular matrix</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Glial cells</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Humans</subject><subject>IL‐1 beta</subject><subject>In vivo methods and tests</subject><subject>Male</subject><subject>MicroRNAs</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miRNA</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>neuroinflammation</subject><subject>Neurological diseases</subject><subject>Neuronal-glial interactions</subject><subject>Non-coding RNA</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Temporal lobe</subject><subject>TGF‐beta</subject><subject>Therapeutic applications</subject><subject>Transcription</subject><subject>Transfection</subject><subject>Transforming growth factor-b1</subject><subject>Young Adult</subject><issn>0894-1491</issn><issn>1098-1136</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp9kc-KFDEQh4Mo7rh68QEk4EWEXlNJ_0kuwrDoujAoiJ5DOl09k6W70ybdq3PzETz6fD6JaXtd1IOnolJfPqr4EfIY2Bkwxl_sO2fOuKgYu0M2wJTMAER5l2yYVHkGuYIT8iDGK8YgNdV9ciIgZ5KLckO-984G__7t9sfXbyA4dZH6awz4ZQwYIzbUDXTxL3XCfvTBdLTzNVIcXYdjPFIzNDRgM1uMdDqkwfrX-YH6lo7BJ_UKT36Pg7O0NXbyIS7Ow9ybgdq5m-bkoCZOwdvjhPEhudeaLuKjm3pKPr5-9eH8TbZ7d3F5vt1lNs8lyxqFFRdNUQirciMBlTGlEY0BaaqmKqSqmYIaagmmUFYVeVPWSpkK03MLSpySl6t3nOseG4vDlE7UY3C9CUftjdN_TwZ30Ht_rUupVJXLJHh2Iwj-04xx0r2LFrvODOjnqDmveCVkIXhCn_6DXvk5DOk8zQUIJQEKkajnK5WCiTFge7sMML0ErpdA9K_AE_zkz_Vv0d8JJwBW4HNK4Pgflb7YXW5X6U9bQbsq</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Korotkov, Anatoly</creator><creator>Broekaart, Diede W. M.</creator><creator>Banchaewa, Leyla</creator><creator>Pustjens, Ben</creator><creator>Scheppingen, Jackelien</creator><creator>Anink, Jasper J.</creator><creator>Baayen, Johannes C.</creator><creator>Idema, Sander</creator><creator>Gorter, Jan A.</creator><creator>Vliet, Erwin A.</creator><creator>Aronica, Eleonora</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>24P</scope><scope>WIN</scope><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>7QL</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3542-3770</orcidid><orcidid>https://orcid.org/0000-0002-0532-4798</orcidid><orcidid>https://orcid.org/0000-0001-5747-3202</orcidid><orcidid>https://orcid.org/0000-0002-8313-6282</orcidid><orcidid>https://orcid.org/0000-0002-4842-0659</orcidid><orcidid>https://orcid.org/0000-0003-3842-1700</orcidid><orcidid>https://orcid.org/0000-0002-0671-857X</orcidid></search><sort><creationdate>202001</creationdate><title>microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes</title><author>Korotkov, Anatoly ; Broekaart, Diede W. M. ; Banchaewa, Leyla ; Pustjens, Ben ; Scheppingen, Jackelien ; Anink, Jasper J. ; Baayen, Johannes C. ; Idema, Sander ; Gorter, Jan A. ; Vliet, Erwin A. ; Aronica, Eleonora</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4480-d9e723d553c94a81e9aa6a3da18a7d7589b091b1b81a59c954d6b99a7e091f193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Animal models</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Astrocytes - metabolism</topic><topic>Astrocytes - pathology</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Drug therapy</topic><topic>Epilepsy</topic><topic>Epilepsy, Temporal Lobe - genetics</topic><topic>Epilepsy, Temporal Lobe - metabolism</topic><topic>Epilepsy, Temporal Lobe - pathology</topic><topic>epileptogenesis</topic><topic>Extracellular matrix</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Glial cells</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Humans</topic><topic>IL‐1 beta</topic><topic>In vivo methods and tests</topic><topic>Male</topic><topic>MicroRNAs</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miRNA</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Neuroglia - metabolism</topic><topic>Neuroglia - pathology</topic><topic>neuroinflammation</topic><topic>Neurological diseases</topic><topic>Neuronal-glial interactions</topic><topic>Non-coding RNA</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Temporal lobe</topic><topic>TGF‐beta</topic><topic>Therapeutic applications</topic><topic>Transcription</topic><topic>Transfection</topic><topic>Transforming growth factor-b1</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Korotkov, Anatoly</creatorcontrib><creatorcontrib>Broekaart, Diede W. M.</creatorcontrib><creatorcontrib>Banchaewa, Leyla</creatorcontrib><creatorcontrib>Pustjens, Ben</creatorcontrib><creatorcontrib>Scheppingen, Jackelien</creatorcontrib><creatorcontrib>Anink, Jasper J.</creatorcontrib><creatorcontrib>Baayen, Johannes C.</creatorcontrib><creatorcontrib>Idema, Sander</creatorcontrib><creatorcontrib>Gorter, Jan A.</creatorcontrib><creatorcontrib>Vliet, Erwin A.</creatorcontrib><creatorcontrib>Aronica, Eleonora</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Glia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Korotkov, Anatoly</au><au>Broekaart, Diede W. M.</au><au>Banchaewa, Leyla</au><au>Pustjens, Ben</au><au>Scheppingen, Jackelien</au><au>Anink, Jasper J.</au><au>Baayen, Johannes C.</au><au>Idema, Sander</au><au>Gorter, Jan A.</au><au>Vliet, Erwin A.</au><au>Aronica, Eleonora</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes</atitle><jtitle>Glia</jtitle><addtitle>Glia</addtitle><date>2020-01</date><risdate>2020</risdate><volume>68</volume><issue>1</issue><spage>60</spage><epage>75</epage><pages>60-75</pages><issn>0894-1491</issn><eissn>1098-1136</eissn><abstract>Temporal lobe epilepsy (TLE) is a chronic neurological disease in humans, which is refractory to pharmacological treatment in about 30% of the patients. Reactive glial cells are thought to play a major role during the development of epilepsy (epileptogenesis) via regulation of brain inflammation and remodeling of the extracellular matrix (ECM). These processes can be regulated by microRNAs (miRs), a class of small non‐coding RNAs, which can control entire gene networks at a post‐transcriptional level. The expression of miRs is known to change dynamically during epileptogenesis. miR‐132 is one of the most commonly upregulated miRs in animal TLE models with important roles shown in neurons. However, the possible role of miR‐132 in glia remains largely unknown. The aim of this study was to characterize the cell‐type specific expression of miR‐132 in the hippocampus of patients with TLE and during epileptogenesis in a rat TLE model. Furthermore, the potential role of miR‐132 was investigated by transfection of human primary cultured astrocytes that were stimulated with the cytokines IL‐1β or TGF‐β1. We showed an increased expression of miR‐132 in the human and rat epileptogenic hippocampus, particularly in glial cells. Transfection of miR‐132 in human primary astrocytes reduced the expression of pro‐epileptogenic COX‐2, IL‐1β, TGF‐β2, CCL2, and MMP3. This suggests that miR‐132, particularly in astrocytes, represents a potential therapeutic target that warrants further in vivo investigation.
Main Points
miR‐132 expression is increased in the epileptogenic human and rat hippocampus.
miR‐132 is expressed by reactive glia.
miR‐132 attenuates expression of pro-epileptogenic factors in cultured human astrocytes.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>31408236</pmid><doi>10.1002/glia.23700</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-3542-3770</orcidid><orcidid>https://orcid.org/0000-0002-0532-4798</orcidid><orcidid>https://orcid.org/0000-0001-5747-3202</orcidid><orcidid>https://orcid.org/0000-0002-8313-6282</orcidid><orcidid>https://orcid.org/0000-0002-4842-0659</orcidid><orcidid>https://orcid.org/0000-0003-3842-1700</orcidid><orcidid>https://orcid.org/0000-0002-0671-857X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Glia, 2020-01, Vol.68 (1), p.60-75 |
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| source | MEDLINE; Access via Wiley Online Library |
| subjects | Adult Aged Aged, 80 and over Animal models Animals Astrocytes Astrocytes - metabolism Astrocytes - pathology Cells, Cultured Cytokines Drug therapy Epilepsy Epilepsy, Temporal Lobe - genetics Epilepsy, Temporal Lobe - metabolism Epilepsy, Temporal Lobe - pathology epileptogenesis Extracellular matrix Female Gene Expression Glial cells Hippocampus Hippocampus - metabolism Hippocampus - pathology Humans IL‐1 beta In vivo methods and tests Male MicroRNAs MicroRNAs - biosynthesis MicroRNAs - genetics Middle Aged miRNA Monocyte chemoattractant protein 1 Neuroglia - metabolism Neuroglia - pathology neuroinflammation Neurological diseases Neuronal-glial interactions Non-coding RNA Rats Rats, Sprague-Dawley Ribonucleic acid RNA Temporal lobe TGF‐beta Therapeutic applications Transcription Transfection Transforming growth factor-b1 Young Adult |
| title | microRNA‐132 is overexpressed in glia in temporal lobe epilepsy and reduces the expression of pro‐epileptogenic factors in human cultured astrocytes |
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