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Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence
The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid...
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Published in: | Journal of molecular neuroscience 2010-03, Vol.40 (3), p.342-352 |
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creator | Costantini, Claudio Lorenzetto, Erika Cellini, Barbara Buffelli, Mario Rossi, Filippo Della-Bianca, Vittorina |
description | The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid β-peptide, the principal event in the pathogenesis of Alzheimer’s disease. Here, by using long-term neuronal cultures as a model of aging, we show that astroglial cells are required to upregulate the expression of IGF1-R in neurons during in vitro senescence. Moreover, evidence is provided that the cross-talk between astrocytes and neurons is independent of cell-to-cell contact, and it is mediated by low molecular weight soluble factor(s) released by astrocytes in culture medium. These results suggest that astrocytes could play an important role in aging and age-related pathological processes. |
doi_str_mv | 10.1007/s12031-009-9305-5 |
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Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid β-peptide, the principal event in the pathogenesis of Alzheimer’s disease. Here, by using long-term neuronal cultures as a model of aging, we show that astroglial cells are required to upregulate the expression of IGF1-R in neurons during in vitro senescence. Moreover, evidence is provided that the cross-talk between astrocytes and neurons is independent of cell-to-cell contact, and it is mediated by low molecular weight soluble factor(s) released by astrocytes in culture medium. These results suggest that astrocytes could play an important role in aging and age-related pathological processes.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-009-9305-5</identifier><identifier>PMID: 19862643</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>Age ; Aging ; Aging - physiology ; Alzheimer's disease ; Animals ; Astrocytes ; Astrocytes - cytology ; Astrocytes - metabolism ; beta -Amyloid ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell culture ; Cells, Cultured ; Cerebral Cortex - cytology ; Cerebral Cortex - physiology ; Coculture Techniques ; Cortex ; Culture Media, Conditioned - metabolism ; Disease ; Insulin ; Insulin-like growth factor I ; Insulin-like growth factors ; Laboratory animals ; Molecular weight ; Nervous system ; Neurochemistry ; Neurodegenerative diseases ; Neurology ; Neurons ; Neurons - cytology ; Neurons - metabolism ; Neurosciences ; Pathology ; Penicillin ; Proteomics ; Rats ; Rats, Sprague-Dawley ; Receptor, IGF Type 1 - metabolism ; Senescence ; Signal transduction ; Signal Transduction - physiology</subject><ispartof>Journal of molecular neuroscience, 2010-03, Vol.40 (3), p.342-352</ispartof><rights>Humana Press 2009</rights><rights>Springer Science+Business Media, LLC 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-fa1fb6eb57a575da0b44c1ec7106859948e8ea955f795eb781669235a1787cc13</citedby><cites>FETCH-LOGICAL-c468t-fa1fb6eb57a575da0b44c1ec7106859948e8ea955f795eb781669235a1787cc13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19862643$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Costantini, Claudio</creatorcontrib><creatorcontrib>Lorenzetto, Erika</creatorcontrib><creatorcontrib>Cellini, Barbara</creatorcontrib><creatorcontrib>Buffelli, Mario</creatorcontrib><creatorcontrib>Rossi, Filippo</creatorcontrib><creatorcontrib>Della-Bianca, Vittorina</creatorcontrib><title>Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid β-peptide, the principal event in the pathogenesis of Alzheimer’s disease. Here, by using long-term neuronal cultures as a model of aging, we show that astroglial cells are required to upregulate the expression of IGF1-R in neurons during in vitro senescence. Moreover, evidence is provided that the cross-talk between astrocytes and neurons is independent of cell-to-cell contact, and it is mediated by low molecular weight soluble factor(s) released by astrocytes in culture medium. These results suggest that astrocytes could play an important role in aging and age-related pathological processes.</description><subject>Age</subject><subject>Aging</subject><subject>Aging - physiology</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - metabolism</subject><subject>beta -Amyloid</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - physiology</subject><subject>Coculture Techniques</subject><subject>Cortex</subject><subject>Culture Media, Conditioned - metabolism</subject><subject>Disease</subject><subject>Insulin</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-like growth factors</subject><subject>Laboratory animals</subject><subject>Molecular weight</subject><subject>Nervous system</subject><subject>Neurochemistry</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Pathology</subject><subject>Penicillin</subject><subject>Proteomics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Senescence</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1DAUhSMEokPhAdggiw2wMPgm8d-yGjrDSCNA5WdrOe5Nm5KxUzsR9Bl4aRxlpEpIiJW9-O65555TFM-BvQXG5LsEJauAMqaprhin_EGxAs41BRDiYbFiSnOqhBYnxZOUbhgroQb1uDgBrUQp6mpV_D5LYwzubsRELvBq6u2IZLxGcv5riJhSFzwJLdn5NPWdp_vuB5JtDD_Ha7KxbgyRQJ5zOMzf17vtBujFG9J58jl2BxvvyDrEsXO2Jx9xisEn8n6Knb_KiuR7l1eTL-gxOfQOnxaPWtsnfHZ8T4tvm_Ov6w90_2m7W5_tqauFGmlroW0ENlxaLvmlZU1dO0AngQnFta4VKrSa81Zqjo1UOQxdVtyCVNI5qE6LV4vuEMPthGk0hy476HvrMUzJaF4LAbXi_yVlVWW41lUmX_5F3oQp-nyGURKyT65khmCBXAwpRWzNsKRkgJm5UbM0anKjZm7UzBZeHIWn5oCX9xPHCjNQLkAa5mAx3m_-t-ofkGuqlA</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Costantini, Claudio</creator><creator>Lorenzetto, Erika</creator><creator>Cellini, Barbara</creator><creator>Buffelli, Mario</creator><creator>Rossi, Filippo</creator><creator>Della-Bianca, Vittorina</creator><general>Humana Press Inc</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20100301</creationdate><title>Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence</title><author>Costantini, Claudio ; Lorenzetto, Erika ; Cellini, Barbara ; Buffelli, Mario ; Rossi, Filippo ; Della-Bianca, Vittorina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-fa1fb6eb57a575da0b44c1ec7106859948e8ea955f795eb781669235a1787cc13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Age</topic><topic>Aging</topic><topic>Aging - physiology</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - metabolism</topic><topic>beta -Amyloid</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - physiology</topic><topic>Coculture Techniques</topic><topic>Cortex</topic><topic>Culture Media, Conditioned - metabolism</topic><topic>Disease</topic><topic>Insulin</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-like growth factors</topic><topic>Laboratory animals</topic><topic>Molecular weight</topic><topic>Nervous system</topic><topic>Neurochemistry</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Pathology</topic><topic>Penicillin</topic><topic>Proteomics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, IGF Type 1 - 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Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Costantini, Claudio</au><au>Lorenzetto, Erika</au><au>Cellini, Barbara</au><au>Buffelli, Mario</au><au>Rossi, Filippo</au><au>Della-Bianca, Vittorina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>40</volume><issue>3</issue><spage>342</spage><epage>352</epage><pages>342-352</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid β-peptide, the principal event in the pathogenesis of Alzheimer’s disease. Here, by using long-term neuronal cultures as a model of aging, we show that astroglial cells are required to upregulate the expression of IGF1-R in neurons during in vitro senescence. Moreover, evidence is provided that the cross-talk between astrocytes and neurons is independent of cell-to-cell contact, and it is mediated by low molecular weight soluble factor(s) released by astrocytes in culture medium. These results suggest that astrocytes could play an important role in aging and age-related pathological processes.</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>19862643</pmid><doi>10.1007/s12031-009-9305-5</doi><tpages>11</tpages></addata></record> |
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subjects | Age Aging Aging - physiology Alzheimer's disease Animals Astrocytes Astrocytes - cytology Astrocytes - metabolism beta -Amyloid Biomedical and Life Sciences Biomedicine Cell Biology Cell culture Cells, Cultured Cerebral Cortex - cytology Cerebral Cortex - physiology Coculture Techniques Cortex Culture Media, Conditioned - metabolism Disease Insulin Insulin-like growth factor I Insulin-like growth factors Laboratory animals Molecular weight Nervous system Neurochemistry Neurodegenerative diseases Neurology Neurons Neurons - cytology Neurons - metabolism Neurosciences Pathology Penicillin Proteomics Rats Rats, Sprague-Dawley Receptor, IGF Type 1 - metabolism Senescence Signal transduction Signal Transduction - physiology |
title | Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence |
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