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GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells

In the rodent ventricular-subventricular zone (V-SVZ) neurons are generated throughout life. They migrate along the rostral migratory stream (RMS) into the olfactory bulb before their final differentiation into interneurons and integration into local circuits. Estrogen receptors (ERs) are steroid ho...

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Autores principales: Haumann, Iris, Sturm, Muriel Anne, Anstötz, Max, Rune, Gabriele M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7200306/
https://www.ncbi.nlm.nih.gov/pubmed/32361597
http://dx.doi.org/10.1016/j.isci.2020.101077
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author Haumann, Iris
Sturm, Muriel Anne
Anstötz, Max
Rune, Gabriele M.
author_facet Haumann, Iris
Sturm, Muriel Anne
Anstötz, Max
Rune, Gabriele M.
author_sort Haumann, Iris
collection PubMed
description In the rodent ventricular-subventricular zone (V-SVZ) neurons are generated throughout life. They migrate along the rostral migratory stream (RMS) into the olfactory bulb before their final differentiation into interneurons and integration into local circuits. Estrogen receptors (ERs) are steroid hormone receptors with important functions in neurogenesis and synaptic plasticity. In this study, we show that the ER GPER1 is expressed in subsets of cells within the V-SVZ of female animals and provide evidence for a potential local estrogen source from aromatase-positive astrocytes surrounding the RMS. Blocking of GPER1 in Matrigel cultures of female animals significantly impairs migration of V-SVZ-derived cells. This outgrowth is accompanied by regulation of phosphorylation of the actin-binding protein cofilin by GPER1 signaling including an involvement of the p21-Ras pathway. Our results point to a prominent role of GPER1 in the initiation of neuronal migration from the V-SVZ to the olfactory bulb.
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spelling pubmed-72003062020-05-07 GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells Haumann, Iris Sturm, Muriel Anne Anstötz, Max Rune, Gabriele M. iScience Article In the rodent ventricular-subventricular zone (V-SVZ) neurons are generated throughout life. They migrate along the rostral migratory stream (RMS) into the olfactory bulb before their final differentiation into interneurons and integration into local circuits. Estrogen receptors (ERs) are steroid hormone receptors with important functions in neurogenesis and synaptic plasticity. In this study, we show that the ER GPER1 is expressed in subsets of cells within the V-SVZ of female animals and provide evidence for a potential local estrogen source from aromatase-positive astrocytes surrounding the RMS. Blocking of GPER1 in Matrigel cultures of female animals significantly impairs migration of V-SVZ-derived cells. This outgrowth is accompanied by regulation of phosphorylation of the actin-binding protein cofilin by GPER1 signaling including an involvement of the p21-Ras pathway. Our results point to a prominent role of GPER1 in the initiation of neuronal migration from the V-SVZ to the olfactory bulb. Elsevier 2020-04-18 /pmc/articles/PMC7200306/ /pubmed/32361597 http://dx.doi.org/10.1016/j.isci.2020.101077 Text en © 2020 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Haumann, Iris
Sturm, Muriel Anne
Anstötz, Max
Rune, Gabriele M.
GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title_full GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title_fullStr GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title_full_unstemmed GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title_short GPER1 Signaling Initiates Migration of Female V-SVZ-Derived Cells
title_sort gper1 signaling initiates migration of female v-svz-derived cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7200306/
https://www.ncbi.nlm.nih.gov/pubmed/32361597
http://dx.doi.org/10.1016/j.isci.2020.101077
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