CNF1 improves astrocytic ability to support neuronal growth and differentiation in vitro
Modulation of cerebral Rho GTPases activity in mice brain by intracerebral administration of Cytotoxic Necrotizing Factor 1 (CNF1) leads to enhanced neurotransmission and synaptic plasticity and improves learning and memory. To gain more insight into the interactions between CNF1 and neuronal cells,...
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| Veröffentlicht in: | PloS one 2012-04, Vol.7 (4), p.e34115 |
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| creator | Malchiodi-Albedi, Fiorella Paradisi, Silvia Di Nottia, Michela Simone, Daiana Travaglione, Sara Falzano, Loredana Guidotti, Marco Frank, Claudio Cutarelli, Alessandro Fabbri, Alessia Fiorentini, Carla |
| description | Modulation of cerebral Rho GTPases activity in mice brain by intracerebral administration of Cytotoxic Necrotizing Factor 1 (CNF1) leads to enhanced neurotransmission and synaptic plasticity and improves learning and memory. To gain more insight into the interactions between CNF1 and neuronal cells, we used primary neuronal and astrocytic cultures from rat embryonic brain to study CNF1 effects on neuronal differentiation, focusing on dendritic tree growth and synapse formation, which are strictly modulated by Rho GTPases. CNF1 profoundly remodeled the cytoskeleton of hippocampal and cortical neurons, which showed philopodia-like, actin-positive projections, thickened and poorly branched dendrites, and a decrease in synapse number. CNF1 removal, however, restored dendritic tree development and synapse formation, suggesting that the toxin can reversibly block neuronal differentiation. On differentiated neurons, CNF1 had a similar effacing effect on synapses. Therefore, a direct interaction with CNF1 is apparently deleterious for neurons. Since astrocytes play a pivotal role in neuronal differentiation and synaptic regulation, we wondered if the beneficial in vivo effect could be mediated by astrocytes. Primary astrocytes from embryonic cortex were treated with CNF1 for 48 hours and used as a substrate for growing hippocampal neurons. Such neurons showed an increased development of neurites, in respect to age-matched controls, with a wider dendritic tree and a richer content in synapses. In CNF1-exposed astrocytes, the production of interleukin 1β, known to reduce dendrite development and complexity in neuronal cultures, was decreased. These results demonstrate that astrocytes, under the influence of CNF1, increase their supporting activity on neuronal growth and differentiation, possibly related to the diminished levels of interleukin 1β. These observations suggest that the enhanced synaptic plasticity and improved learning and memory described in CNF1-injected mice are probably mediated by astrocytes. |
| doi_str_mv | 10.1371/journal.pone.0034115 |
| format | Article |
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To gain more insight into the interactions between CNF1 and neuronal cells, we used primary neuronal and astrocytic cultures from rat embryonic brain to study CNF1 effects on neuronal differentiation, focusing on dendritic tree growth and synapse formation, which are strictly modulated by Rho GTPases. CNF1 profoundly remodeled the cytoskeleton of hippocampal and cortical neurons, which showed philopodia-like, actin-positive projections, thickened and poorly branched dendrites, and a decrease in synapse number. CNF1 removal, however, restored dendritic tree development and synapse formation, suggesting that the toxin can reversibly block neuronal differentiation. On differentiated neurons, CNF1 had a similar effacing effect on synapses. Therefore, a direct interaction with CNF1 is apparently deleterious for neurons. Since astrocytes play a pivotal role in neuronal differentiation and synaptic regulation, we wondered if the beneficial in vivo effect could be mediated by astrocytes. Primary astrocytes from embryonic cortex were treated with CNF1 for 48 hours and used as a substrate for growing hippocampal neurons. Such neurons showed an increased development of neurites, in respect to age-matched controls, with a wider dendritic tree and a richer content in synapses. In CNF1-exposed astrocytes, the production of interleukin 1β, known to reduce dendrite development and complexity in neuronal cultures, was decreased. These results demonstrate that astrocytes, under the influence of CNF1, increase their supporting activity on neuronal growth and differentiation, possibly related to the diminished levels of interleukin 1β. These observations suggest that the enhanced synaptic plasticity and improved learning and memory described in CNF1-injected mice are probably mediated by astrocytes.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0034115</identifier><identifier>PMID: 22523545</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Actin ; Animals ; Apoptosis ; Astrocytes ; Astrocytes - drug effects ; Astrocytes - physiology ; Axons ; Bacterial Toxins - pharmacology ; Biology ; Brain ; Brain research ; Cell Differentiation - drug effects ; Cells, Cultured ; Coculture Techniques ; Cortex ; Cytoskeleton ; Cytotoxic necrotizing factor 1 ; Cytotoxicity ; Dendrites ; Dendritic Cells - drug effects ; Dendritic structure ; Differentiation ; E coli ; Embryos ; Escherichia coli ; Escherichia coli Proteins - pharmacology ; G proteins ; Growth ; Hippocampus ; Inflammation ; Interleukin-1beta - biosynthesis ; Interleukins ; Learning ; Memory ; Mice ; Morphogenesis ; Muscle proteins ; Neurodegeneration ; Neurogenesis ; Neurogenesis - drug effects ; Neurons ; Neurons - drug effects ; Neurons - physiology ; Neurophysiology ; Neurosciences ; Neurotransmission ; Pathogenesis ; Plasticity ; Rats ; Rats, Wistar ; rho GTP-Binding Proteins - antagonists & inhibitors ; rho GTP-Binding Proteins - metabolism ; Schizophrenia ; Signal transduction ; Synapses ; Synapses - drug effects ; Synaptic plasticity ; Synaptogenesis ; Toxins ; Traumatic brain injury ; Tree growth ; Trees ; Trends</subject><ispartof>PloS one, 2012-04, Vol.7 (4), p.e34115</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Malchiodi-Albedi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Malchiodi-Albedi et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-8122c5f041a6a9ca1eb1d452bed39b13f81cb7560906866e7e83ad068e7b27073</citedby><cites>FETCH-LOGICAL-c692t-8122c5f041a6a9ca1eb1d452bed39b13f81cb7560906866e7e83ad068e7b27073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327681/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327681/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22523545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Landsberger, Nicoletta</contributor><creatorcontrib>Malchiodi-Albedi, Fiorella</creatorcontrib><creatorcontrib>Paradisi, Silvia</creatorcontrib><creatorcontrib>Di Nottia, Michela</creatorcontrib><creatorcontrib>Simone, Daiana</creatorcontrib><creatorcontrib>Travaglione, Sara</creatorcontrib><creatorcontrib>Falzano, Loredana</creatorcontrib><creatorcontrib>Guidotti, Marco</creatorcontrib><creatorcontrib>Frank, Claudio</creatorcontrib><creatorcontrib>Cutarelli, Alessandro</creatorcontrib><creatorcontrib>Fabbri, Alessia</creatorcontrib><creatorcontrib>Fiorentini, Carla</creatorcontrib><title>CNF1 improves astrocytic ability to support neuronal growth and differentiation in vitro</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Modulation of cerebral Rho GTPases activity in mice brain by intracerebral administration of Cytotoxic Necrotizing Factor 1 (CNF1) leads to enhanced neurotransmission and synaptic plasticity and improves learning and memory. To gain more insight into the interactions between CNF1 and neuronal cells, we used primary neuronal and astrocytic cultures from rat embryonic brain to study CNF1 effects on neuronal differentiation, focusing on dendritic tree growth and synapse formation, which are strictly modulated by Rho GTPases. CNF1 profoundly remodeled the cytoskeleton of hippocampal and cortical neurons, which showed philopodia-like, actin-positive projections, thickened and poorly branched dendrites, and a decrease in synapse number. CNF1 removal, however, restored dendritic tree development and synapse formation, suggesting that the toxin can reversibly block neuronal differentiation. On differentiated neurons, CNF1 had a similar effacing effect on synapses. Therefore, a direct interaction with CNF1 is apparently deleterious for neurons. Since astrocytes play a pivotal role in neuronal differentiation and synaptic regulation, we wondered if the beneficial in vivo effect could be mediated by astrocytes. Primary astrocytes from embryonic cortex were treated with CNF1 for 48 hours and used as a substrate for growing hippocampal neurons. Such neurons showed an increased development of neurites, in respect to age-matched controls, with a wider dendritic tree and a richer content in synapses. In CNF1-exposed astrocytes, the production of interleukin 1β, known to reduce dendrite development and complexity in neuronal cultures, was decreased. These results demonstrate that astrocytes, under the influence of CNF1, increase their supporting activity on neuronal growth and differentiation, possibly related to the diminished levels of interleukin 1β. These observations suggest that the enhanced synaptic plasticity and improved learning and memory described in CNF1-injected mice are probably mediated by astrocytes.</description><subject>Actin</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - physiology</subject><subject>Axons</subject><subject>Bacterial Toxins - pharmacology</subject><subject>Biology</subject><subject>Brain</subject><subject>Brain research</subject><subject>Cell Differentiation - drug effects</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Cortex</subject><subject>Cytoskeleton</subject><subject>Cytotoxic necrotizing factor 1</subject><subject>Cytotoxicity</subject><subject>Dendrites</subject><subject>Dendritic Cells - drug effects</subject><subject>Dendritic structure</subject><subject>Differentiation</subject><subject>E coli</subject><subject>Embryos</subject><subject>Escherichia coli</subject><subject>Escherichia coli Proteins - 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To gain more insight into the interactions between CNF1 and neuronal cells, we used primary neuronal and astrocytic cultures from rat embryonic brain to study CNF1 effects on neuronal differentiation, focusing on dendritic tree growth and synapse formation, which are strictly modulated by Rho GTPases. CNF1 profoundly remodeled the cytoskeleton of hippocampal and cortical neurons, which showed philopodia-like, actin-positive projections, thickened and poorly branched dendrites, and a decrease in synapse number. CNF1 removal, however, restored dendritic tree development and synapse formation, suggesting that the toxin can reversibly block neuronal differentiation. On differentiated neurons, CNF1 had a similar effacing effect on synapses. Therefore, a direct interaction with CNF1 is apparently deleterious for neurons. Since astrocytes play a pivotal role in neuronal differentiation and synaptic regulation, we wondered if the beneficial in vivo effect could be mediated by astrocytes. Primary astrocytes from embryonic cortex were treated with CNF1 for 48 hours and used as a substrate for growing hippocampal neurons. Such neurons showed an increased development of neurites, in respect to age-matched controls, with a wider dendritic tree and a richer content in synapses. In CNF1-exposed astrocytes, the production of interleukin 1β, known to reduce dendrite development and complexity in neuronal cultures, was decreased. These results demonstrate that astrocytes, under the influence of CNF1, increase their supporting activity on neuronal growth and differentiation, possibly related to the diminished levels of interleukin 1β. These observations suggest that the enhanced synaptic plasticity and improved learning and memory described in CNF1-injected mice are probably mediated by astrocytes.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22523545</pmid><doi>10.1371/journal.pone.0034115</doi><tpages>e34115</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-04, Vol.7 (4), p.e34115 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1324570052 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Actin Animals Apoptosis Astrocytes Astrocytes - drug effects Astrocytes - physiology Axons Bacterial Toxins - pharmacology Biology Brain Brain research Cell Differentiation - drug effects Cells, Cultured Coculture Techniques Cortex Cytoskeleton Cytotoxic necrotizing factor 1 Cytotoxicity Dendrites Dendritic Cells - drug effects Dendritic structure Differentiation E coli Embryos Escherichia coli Escherichia coli Proteins - pharmacology G proteins Growth Hippocampus Inflammation Interleukin-1beta - biosynthesis Interleukins Learning Memory Mice Morphogenesis Muscle proteins Neurodegeneration Neurogenesis Neurogenesis - drug effects Neurons Neurons - drug effects Neurons - physiology Neurophysiology Neurosciences Neurotransmission Pathogenesis Plasticity Rats Rats, Wistar rho GTP-Binding Proteins - antagonists & inhibitors rho GTP-Binding Proteins - metabolism Schizophrenia Signal transduction Synapses Synapses - drug effects Synaptic plasticity Synaptogenesis Toxins Traumatic brain injury Tree growth Trees Trends |
| title | CNF1 improves astrocytic ability to support neuronal growth and differentiation in vitro |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T14%3A18%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CNF1%20improves%20astrocytic%20ability%20to%20support%20neuronal%20growth%20and%20differentiation%20in%20vitro&rft.jtitle=PloS%20one&rft.au=Malchiodi-Albedi,%20Fiorella&rft.date=2012-04-16&rft.volume=7&rft.issue=4&rft.spage=e34115&rft.pages=e34115-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0034115&rft_dat=%3Cgale_plos_%3EA477082386%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1324570052&rft_id=info:pmid/22523545&rft_galeid=A477082386&rft_doaj_id=oai_doaj_org_article_f2ffea6c7046407fb2bb6371c212061f&rfr_iscdi=true |