The effect of interferon-β on mouse neural progenitor cell survival and differentiation
Interferon-β (IFN-β) is a mainstay therapy for relapse-remitting multiple sclerosis (MS). However, the direct effects of IFN-β on the central nervous system (CNS) are not well understood. To determine whether IFN-β has direct neuroprotective effects on CNS cells, we treated adult mouse neural progen...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2009-10, Vol.388 (2), p.181-186 |
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| creator | Hirsch, Marek Knight, Julia Tobita, Mari Soltys, John Panitch, Hillel Mao-Draayer, Yang |
| description | Interferon-β (IFN-β) is a mainstay therapy for relapse-remitting multiple sclerosis (MS). However, the direct effects of IFN-β on the central nervous system (CNS) are not well understood. To determine whether IFN-β has direct neuroprotective effects on CNS cells, we treated adult mouse neural progenitor cells (NPCs)
in vitro with IFN-β and examined the effects on proliferation, apoptosis, and differentiation. We found that mouse NPCs express high levels of IFNα/β receptor (IFNAR). In response to IFN-β treatment, no effect was observed on differentiation or proliferation. However, IFN-β treated mouse NPCs demonstrated decreased apoptosis upon growth factor withdrawal. Pathway-specific polymerase chain reaction (PCR) arrays demonstrated that IFN-β treatment upregulated the STAT 1 and 2 signaling pathway, as well as GFRA2, NOD1, Caspases 1 and 12, and TNFSF10. These results suggest that IFN-β can directly affect NPC survival, possibly playing a neuroprotective role in the CNS by modulating neurotrophic factors. |
| doi_str_mv | 10.1016/j.bbrc.2009.07.073 |
| format | Article |
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in vitro with IFN-β and examined the effects on proliferation, apoptosis, and differentiation. We found that mouse NPCs express high levels of IFNα/β receptor (IFNAR). In response to IFN-β treatment, no effect was observed on differentiation or proliferation. However, IFN-β treated mouse NPCs demonstrated decreased apoptosis upon growth factor withdrawal. Pathway-specific polymerase chain reaction (PCR) arrays demonstrated that IFN-β treatment upregulated the STAT 1 and 2 signaling pathway, as well as GFRA2, NOD1, Caspases 1 and 12, and TNFSF10. These results suggest that IFN-β can directly affect NPC survival, possibly playing a neuroprotective role in the CNS by modulating neurotrophic factors.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2009.07.073</identifier><identifier>PMID: 19619508</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cell Survival - drug effects ; Cells, Cultured ; Gene Expression Regulation ; IFNα/β receptor ; Interferon-beta - pharmacology ; Interferon-β ; Mice ; Mouse neural progenitor cells ; Multiple sclerosis ; Neurogenesis - drug effects ; Neurogenesis - genetics ; Neurogenesis - physiology ; Neurons - drug effects ; Neurons - physiology ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Receptor, Interferon alpha-beta - biosynthesis ; STAT signaling ; Stem Cells - drug effects ; Stem Cells - physiology</subject><ispartof>Biochemical and biophysical research communications, 2009-10, Vol.388 (2), p.181-186</ispartof><rights>2009 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-ac0df3517bf1c85c07fca56476b61c98780777ebcc2d1b9c5140d239852e6833</citedby><cites>FETCH-LOGICAL-c484t-ac0df3517bf1c85c07fca56476b61c98780777ebcc2d1b9c5140d239852e6833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X09014211$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19619508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirsch, Marek</creatorcontrib><creatorcontrib>Knight, Julia</creatorcontrib><creatorcontrib>Tobita, Mari</creatorcontrib><creatorcontrib>Soltys, John</creatorcontrib><creatorcontrib>Panitch, Hillel</creatorcontrib><creatorcontrib>Mao-Draayer, Yang</creatorcontrib><title>The effect of interferon-β on mouse neural progenitor cell survival and differentiation</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Interferon-β (IFN-β) is a mainstay therapy for relapse-remitting multiple sclerosis (MS). However, the direct effects of IFN-β on the central nervous system (CNS) are not well understood. To determine whether IFN-β has direct neuroprotective effects on CNS cells, we treated adult mouse neural progenitor cells (NPCs)
in vitro with IFN-β and examined the effects on proliferation, apoptosis, and differentiation. We found that mouse NPCs express high levels of IFNα/β receptor (IFNAR). In response to IFN-β treatment, no effect was observed on differentiation or proliferation. However, IFN-β treated mouse NPCs demonstrated decreased apoptosis upon growth factor withdrawal. Pathway-specific polymerase chain reaction (PCR) arrays demonstrated that IFN-β treatment upregulated the STAT 1 and 2 signaling pathway, as well as GFRA2, NOD1, Caspases 1 and 12, and TNFSF10. These results suggest that IFN-β can directly affect NPC survival, possibly playing a neuroprotective role in the CNS by modulating neurotrophic factors.</description><subject>Animals</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Gene Expression Regulation</subject><subject>IFNα/β receptor</subject><subject>Interferon-beta - pharmacology</subject><subject>Interferon-β</subject><subject>Mice</subject><subject>Mouse neural progenitor cells</subject><subject>Multiple sclerosis</subject><subject>Neurogenesis - drug effects</subject><subject>Neurogenesis - genetics</subject><subject>Neurogenesis - physiology</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Receptor, Interferon alpha-beta - biosynthesis</subject><subject>STAT signaling</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - physiology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9q3DAQxkVJabZpXyCHoFNu3oxsS7KgFELon0Cglz3kJmR5lGjZlbaSvZDXyoPkmSqzS9tcAgM6zDffN6MfIecMlgyYuFov-z7ZZQ2gliBLNe_IgoGCqmbQnpAFAIiqVuz-lHzMeQ3AWCvUB3LKlGCKQ7cg96tHpOgc2pFGR30YMTlMMVQvzzQGuo1TRhpwSmZDdyk-YPBjTNTiZkPzlPZ-XxomDHTwxSVhGL0ZfQyfyHtnNhk_H98zsvr-bXXzs7r79eP25vqusm3XjpWxMLiGM9k7ZjtuQTpruGil6AWzqpMdSCmxt7YeWK8sZy0MdaM6XqPomuaMfD3Y7qZ-i4Mt-WVTvUt-a9KTjsbr153gH_VD3GvOoW2hKwaXR4MUf0-YR731eb7OBCy36xokCMHnpPogtCnmnND9DWGgZx56rWceeuahQZaahy7-X-_fyBFAEXw5CLD80d5j0tl6DBYHnwoTPUT_lv8f3WmfGw</recordid><startdate>20091016</startdate><enddate>20091016</enddate><creator>Hirsch, Marek</creator><creator>Knight, Julia</creator><creator>Tobita, Mari</creator><creator>Soltys, John</creator><creator>Panitch, Hillel</creator><creator>Mao-Draayer, Yang</creator><general>Elsevier Inc</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20091016</creationdate><title>The effect of interferon-β on mouse neural progenitor cell survival and differentiation</title><author>Hirsch, Marek ; 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However, the direct effects of IFN-β on the central nervous system (CNS) are not well understood. To determine whether IFN-β has direct neuroprotective effects on CNS cells, we treated adult mouse neural progenitor cells (NPCs)
in vitro with IFN-β and examined the effects on proliferation, apoptosis, and differentiation. We found that mouse NPCs express high levels of IFNα/β receptor (IFNAR). In response to IFN-β treatment, no effect was observed on differentiation or proliferation. However, IFN-β treated mouse NPCs demonstrated decreased apoptosis upon growth factor withdrawal. Pathway-specific polymerase chain reaction (PCR) arrays demonstrated that IFN-β treatment upregulated the STAT 1 and 2 signaling pathway, as well as GFRA2, NOD1, Caspases 1 and 12, and TNFSF10. These results suggest that IFN-β can directly affect NPC survival, possibly playing a neuroprotective role in the CNS by modulating neurotrophic factors.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19619508</pmid><doi>10.1016/j.bbrc.2009.07.073</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Survival - drug effects Cells, Cultured Gene Expression Regulation IFNα/β receptor Interferon-beta - pharmacology Interferon-β Mice Mouse neural progenitor cells Multiple sclerosis Neurogenesis - drug effects Neurogenesis - genetics Neurogenesis - physiology Neurons - drug effects Neurons - physiology Neuroprotection Neuroprotective Agents - pharmacology Receptor, Interferon alpha-beta - biosynthesis STAT signaling Stem Cells - drug effects Stem Cells - physiology |
| title | The effect of interferon-β on mouse neural progenitor cell survival and differentiation |
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