LIF–IGF Axis Contributes to the Proliferation of Neural Progenitor Cells in Developing Rat Cerebrum
In rodent models, leukemia inhibitory factor (LIF) is involved in cerebral development via the placenta, and maternal immune activation is linked to psychiatric disorders in the child. However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA micr...
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| Veröffentlicht in: | International journal of molecular sciences 2022-10, Vol.23 (21), p.13199 |
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| creator | Takata, Sho Sakata-Haga, Hiromi Shimada, Hiroki Tsukada, Tsuyoshi Sakai, Daisuke Shoji, Hiroki Tomosugi, Mitsuhiro Nakamura, Yuka Ishigaki, Yasuhito Iizuka, Hideaki Hayashi, Yasuhiko Hatta, Toshihisa |
| description | In rodent models, leukemia inhibitory factor (LIF) is involved in cerebral development via the placenta, and maternal immune activation is linked to psychiatric disorders in the child. However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA microarray analysis and quantitative RT-PCR on the fetal cerebrum after maternal intraperitoneal or fetal intracerebral ventricular injection of LIF at day 14.5 (E14.5) and determined that the expression of insulin-like growth factors (IGF)-1 and -2 was induced by LIF. Physiological IGF-1 and IGF-2 levels in fetal cerebrospinal fluid (CSF) increased from E15.5 to E17.5, following the physiological surge of LIF levels in CSF at E15.5. Immunostaining showed that IGF-1 was expressed in the cerebrum at E15.5 to E19.5 and IGF-2 at E15.5 to E17.5 and that IGF-1 receptor and insulin receptor were co-expressed in NPCs. Further, LIF treatment enhanced cultured NPC proliferation, which was reduced by picropodophyllin, an IGF-1 receptor inhibitor, even under LIF supplementation. Our findings suggest that IGF expression and release from the NPCs of the fetal cerebrum in fetal CSF is induced by LIF, thus supporting the involvement of the LIF–IGF axis in cerebral cortical development in an autocrine/paracrine manner. |
| doi_str_mv | 10.3390/ijms232113199 |
| format | Article |
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However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA microarray analysis and quantitative RT-PCR on the fetal cerebrum after maternal intraperitoneal or fetal intracerebral ventricular injection of LIF at day 14.5 (E14.5) and determined that the expression of insulin-like growth factors (IGF)-1 and -2 was induced by LIF. Physiological IGF-1 and IGF-2 levels in fetal cerebrospinal fluid (CSF) increased from E15.5 to E17.5, following the physiological surge of LIF levels in CSF at E15.5. Immunostaining showed that IGF-1 was expressed in the cerebrum at E15.5 to E19.5 and IGF-2 at E15.5 to E17.5 and that IGF-1 receptor and insulin receptor were co-expressed in NPCs. Further, LIF treatment enhanced cultured NPC proliferation, which was reduced by picropodophyllin, an IGF-1 receptor inhibitor, even under LIF supplementation. Our findings suggest that IGF expression and release from the NPCs of the fetal cerebrum in fetal CSF is induced by LIF, thus supporting the involvement of the LIF–IGF axis in cerebral cortical development in an autocrine/paracrine manner.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms232113199</identifier><identifier>PMID: 36361987</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Animal models ; Autocrine signalling ; Cell proliferation ; Cerebrospinal fluid ; Cerebrum ; DNA chips ; DNA microarrays ; Fetuses ; Gene expression ; Growth factors ; Immune response ; Insulin ; Insulin-like growth factor I ; Insulin-like growth factors ; Leukemia ; Leukemia inhibitory factor ; Localization ; Mental disorders ; Neural stem cells ; Neurogenesis ; Paracrine signalling ; Physiological effects ; Physiology ; Progenitor cells ; Ventricle</subject><ispartof>International journal of molecular sciences, 2022-10, Vol.23 (21), p.13199</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA microarray analysis and quantitative RT-PCR on the fetal cerebrum after maternal intraperitoneal or fetal intracerebral ventricular injection of LIF at day 14.5 (E14.5) and determined that the expression of insulin-like growth factors (IGF)-1 and -2 was induced by LIF. Physiological IGF-1 and IGF-2 levels in fetal cerebrospinal fluid (CSF) increased from E15.5 to E17.5, following the physiological surge of LIF levels in CSF at E15.5. Immunostaining showed that IGF-1 was expressed in the cerebrum at E15.5 to E19.5 and IGF-2 at E15.5 to E17.5 and that IGF-1 receptor and insulin receptor were co-expressed in NPCs. Further, LIF treatment enhanced cultured NPC proliferation, which was reduced by picropodophyllin, an IGF-1 receptor inhibitor, even under LIF supplementation. Our findings suggest that IGF expression and release from the NPCs of the fetal cerebrum in fetal CSF is induced by LIF, thus supporting the involvement of the LIF–IGF axis in cerebral cortical development in an autocrine/paracrine manner.</description><subject>Animal models</subject><subject>Autocrine signalling</subject><subject>Cell proliferation</subject><subject>Cerebrospinal fluid</subject><subject>Cerebrum</subject><subject>DNA chips</subject><subject>DNA microarrays</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Immune response</subject><subject>Insulin</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-like growth factors</subject><subject>Leukemia</subject><subject>Leukemia inhibitory factor</subject><subject>Localization</subject><subject>Mental disorders</subject><subject>Neural stem cells</subject><subject>Neurogenesis</subject><subject>Paracrine signalling</subject><subject>Physiological effects</subject><subject>Physiology</subject><subject>Progenitor cells</subject><subject>Ventricle</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1q20AUhYeSELtOlt0PZJON2vmR5mcTME7sGkxbSrMeRtKVM0bSODOjkOz6Dn3DPklkYkqT1b3c-3E4h4PQJ0o-c67JF7frIuOMUk61_oCmNGcsI0TIk__2CfoY446QESz0GZpwwQXVSk4RbNbLv7__rFdLPH9yES98n4IrhwQRJ4_TPeAfwbeugWCT8z32Df4GQ7Dt4b6F3iUf8ALaNmLX4xt4hNbvXb_FP20a7wHKMHTn6LSxbYSL45yhu-Xtr8XXbPN9tV7MN1mVFyplVZlLeTDNiQBS5yC4tLVqpFVWV7WSRAGAYFTQHAoo6tyqimtZKgaUlBWfoetX3f1QdlBXMIaxrdkH19nwbLx15u2nd_dm6x-NFoVmOh8Fro4CwT8MEJPpXKzGdLYHP0TDJC-UKBTTI3r5Dt35IfRjvAOVC66FUiOVvVJV8DEGaP6ZocQcCjRvCuQvUyOOdA</recordid><startdate>20221030</startdate><enddate>20221030</enddate><creator>Takata, Sho</creator><creator>Sakata-Haga, Hiromi</creator><creator>Shimada, Hiroki</creator><creator>Tsukada, Tsuyoshi</creator><creator>Sakai, Daisuke</creator><creator>Shoji, Hiroki</creator><creator>Tomosugi, Mitsuhiro</creator><creator>Nakamura, Yuka</creator><creator>Ishigaki, Yasuhito</creator><creator>Iizuka, Hideaki</creator><creator>Hayashi, Yasuhiko</creator><creator>Hatta, Toshihisa</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4928-0301</orcidid><orcidid>https://orcid.org/0000-0003-1012-8430</orcidid><orcidid>https://orcid.org/0000-0001-7992-2793</orcidid><orcidid>https://orcid.org/0000-0001-5102-7690</orcidid><orcidid>https://orcid.org/0000-0001-5538-4927</orcidid><orcidid>https://orcid.org/0000-0002-8183-9080</orcidid><orcidid>https://orcid.org/0000-0001-5998-3329</orcidid></search><sort><creationdate>20221030</creationdate><title>LIF–IGF Axis Contributes to the Proliferation of Neural Progenitor Cells in Developing Rat Cerebrum</title><author>Takata, Sho ; 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| subjects | Animal models Autocrine signalling Cell proliferation Cerebrospinal fluid Cerebrum DNA chips DNA microarrays Fetuses Gene expression Growth factors Immune response Insulin Insulin-like growth factor I Insulin-like growth factors Leukemia Leukemia inhibitory factor Localization Mental disorders Neural stem cells Neurogenesis Paracrine signalling Physiological effects Physiology Progenitor cells Ventricle |
| title | LIF–IGF Axis Contributes to the Proliferation of Neural Progenitor Cells in Developing Rat Cerebrum |
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