256. Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector
The bone marrow stromal cells (MSCs), including the primitive pluriopotent mesenchymal stem cells (PMSCs) and the multipotent adult progenitor cells (MAPCs), are attractive targets for cell and gene therapy for various central nervous system disorders.Material and method: For gene modification of MS...
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| Veröffentlicht in: | Molecular therapy 2006-05, Vol.13 (S1), p.S98-S99 |
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| creator | Nonoguchi, Naosuke Zhao, Ming-Zhu Ikeda, Naokado Miki, Yoshihito Furutama, Daisuke Kimura, Fumiharu Dezawa, Mari Funakoshi, Hiroshi Coffin, Robert S. Miyatake, Shin-ichi Kuroiwa, Toshihiko |
| description | The bone marrow stromal cells (MSCs), including the primitive pluriopotent mesenchymal stem cells (PMSCs) and the multipotent adult progenitor cells (MAPCs), are attractive targets for cell and gene therapy for various central nervous system disorders.Material and method: For gene modification of MSCs, we used a replication-incompetent HSV-1 vector "1764/4-", triple-deletion mutant of the ICP4, ICP34.5, and VP16. This vector has very high ability of gene transduction to MSC, 70-75% at MOI 10 and 95% at MOI 50, and its expression can carry on at least one month at high level. Two kinds of vectors expressing HGF and FGF-2 were prepared for this study. FGF-2 vector contains the signal sequence of Interleukin-2 (IL-2ss) ahead of FGF-2 gene to enhance its extracellular secretion, because native FGF2 gene don't have the excretion signal. Native MSCs, HGF-MSCs, IL2ss+FGF-2-MSCs and PBS were administered directly into the lesioned brain 24 hours after transient middle cerebral artery occlusion (MCAO) of adult Wister rats.Results: At day 14, each gene modified MSC group showed significant improvement in modified neurological severity score (mNSS) and apparent decreasing of infarct volume compared with native MSC or sham-operated group. (p |
| doi_str_mv | 10.1016/j.ymthe.2006.08.283 |
| format | Article |
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Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>ProQuest Central UK/Ireland</source><source>Alma/SFX Local Collection</source><creator>Nonoguchi, Naosuke ; Zhao, Ming-Zhu ; Ikeda, Naokado ; Miki, Yoshihito ; Furutama, Daisuke ; Kimura, Fumiharu ; Dezawa, Mari ; Funakoshi, Hiroshi ; Coffin, Robert S. ; Miyatake, Shin-ichi ; Kuroiwa, Toshihiko</creator><creatorcontrib>Nonoguchi, Naosuke ; Zhao, Ming-Zhu ; Ikeda, Naokado ; Miki, Yoshihito ; Furutama, Daisuke ; Kimura, Fumiharu ; Dezawa, Mari ; Funakoshi, Hiroshi ; Coffin, Robert S. ; Miyatake, Shin-ichi ; Kuroiwa, Toshihiko</creatorcontrib><description>The bone marrow stromal cells (MSCs), including the primitive pluriopotent mesenchymal stem cells (PMSCs) and the multipotent adult progenitor cells (MAPCs), are attractive targets for cell and gene therapy for various central nervous system disorders.Material and method: For gene modification of MSCs, we used a replication-incompetent HSV-1 vector "1764/4-", triple-deletion mutant of the ICP4, ICP34.5, and VP16. This vector has very high ability of gene transduction to MSC, 70-75% at MOI 10 and 95% at MOI 50, and its expression can carry on at least one month at high level. Two kinds of vectors expressing HGF and FGF-2 were prepared for this study. FGF-2 vector contains the signal sequence of Interleukin-2 (IL-2ss) ahead of FGF-2 gene to enhance its extracellular secretion, because native FGF2 gene don't have the excretion signal. Native MSCs, HGF-MSCs, IL2ss+FGF-2-MSCs and PBS were administered directly into the lesioned brain 24 hours after transient middle cerebral artery occlusion (MCAO) of adult Wister rats.Results: At day 14, each gene modified MSC group showed significant improvement in modified neurological severity score (mNSS) and apparent decreasing of infarct volume compared with native MSC or sham-operated group. (p<0.05). HGF and FGF-2 expression in vivo were strongly kept through the experimental period. In HGF modified MSC-treated group, the MAP-2 positive cell% tends to increase and the TUNEL positive cell% decrease in the ischemic boundary zone (IBZ). The transdifferentiation of transplanted MSCs to central nervous system cell phenotypes was also checked. Most of the transdifferentiated phenotype was GFAP- positive, and the Nestin-positive cells were scarcely able to find out in the host brain.Discussion and Conclusion: By using the replication- incompetent HSV-1 vector, MSCs can be efficiently engineered to secrete a series of various cytokines in large quantities and in the long term in vitro and in vivo that could potentially treat the ischemic stroke of the brain. HGF and FGF-2 gene-transferred MSCs, achieved the remarkable amelioration of neurological symptoms and apparent decreasing of infarct volume comparison with native MSCs in rat MCAO model. It would be appeared that the main mechanism of these therapeutic effects is the neuroprotection (anti-apoptotic effect) in IBZ by various abundant cytokines secreted from gene engineered MSCs. We will present our detail data of the study and the perspective of this therapeutic strategy.</description><identifier>ISSN: 1525-0016</identifier><identifier>EISSN: 1525-0024</identifier><identifier>DOI: 10.1016/j.ymthe.2006.08.283</identifier><language>eng</language><publisher>Milwaukee: Elsevier Limited</publisher><subject>Alzheimer's disease ; Antioxidants ; Apoptosis ; Bone marrow ; Cytokines ; Drug dosages ; Enzymes ; Gene therapy ; Herpes viruses ; Internal medicine ; Ischemia ; Medical schools ; Medicine ; Nervous system ; Neurons ; Neurosciences ; Neurosurgery ; Oxidative stress ; Performance evaluation ; Vectors (Biology)</subject><ispartof>Molecular therapy, 2006-05, Vol.13 (S1), p.S98-S99</ispartof><rights>Copyright Nature Publishing Group May 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1673-a8620a2414430bdd14b35f3a98078648668079a64679a2715ad795bd6692f2373</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1792801990?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,64361,64365,72215</link.rule.ids></links><search><creatorcontrib>Nonoguchi, Naosuke</creatorcontrib><creatorcontrib>Zhao, Ming-Zhu</creatorcontrib><creatorcontrib>Ikeda, Naokado</creatorcontrib><creatorcontrib>Miki, Yoshihito</creatorcontrib><creatorcontrib>Furutama, Daisuke</creatorcontrib><creatorcontrib>Kimura, Fumiharu</creatorcontrib><creatorcontrib>Dezawa, Mari</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Coffin, Robert S.</creatorcontrib><creatorcontrib>Miyatake, Shin-ichi</creatorcontrib><creatorcontrib>Kuroiwa, Toshihiko</creatorcontrib><title>256. Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector</title><title>Molecular therapy</title><description>The bone marrow stromal cells (MSCs), including the primitive pluriopotent mesenchymal stem cells (PMSCs) and the multipotent adult progenitor cells (MAPCs), are attractive targets for cell and gene therapy for various central nervous system disorders.Material and method: For gene modification of MSCs, we used a replication-incompetent HSV-1 vector "1764/4-", triple-deletion mutant of the ICP4, ICP34.5, and VP16. This vector has very high ability of gene transduction to MSC, 70-75% at MOI 10 and 95% at MOI 50, and its expression can carry on at least one month at high level. Two kinds of vectors expressing HGF and FGF-2 were prepared for this study. FGF-2 vector contains the signal sequence of Interleukin-2 (IL-2ss) ahead of FGF-2 gene to enhance its extracellular secretion, because native FGF2 gene don't have the excretion signal. Native MSCs, HGF-MSCs, IL2ss+FGF-2-MSCs and PBS were administered directly into the lesioned brain 24 hours after transient middle cerebral artery occlusion (MCAO) of adult Wister rats.Results: At day 14, each gene modified MSC group showed significant improvement in modified neurological severity score (mNSS) and apparent decreasing of infarct volume compared with native MSC or sham-operated group. (p<0.05). HGF and FGF-2 expression in vivo were strongly kept through the experimental period. In HGF modified MSC-treated group, the MAP-2 positive cell% tends to increase and the TUNEL positive cell% decrease in the ischemic boundary zone (IBZ). The transdifferentiation of transplanted MSCs to central nervous system cell phenotypes was also checked. Most of the transdifferentiated phenotype was GFAP- positive, and the Nestin-positive cells were scarcely able to find out in the host brain.Discussion and Conclusion: By using the replication- incompetent HSV-1 vector, MSCs can be efficiently engineered to secrete a series of various cytokines in large quantities and in the long term in vitro and in vivo that could potentially treat the ischemic stroke of the brain. HGF and FGF-2 gene-transferred MSCs, achieved the remarkable amelioration of neurological symptoms and apparent decreasing of infarct volume comparison with native MSCs in rat MCAO model. It would be appeared that the main mechanism of these therapeutic effects is the neuroprotection (anti-apoptotic effect) in IBZ by various abundant cytokines secreted from gene engineered MSCs. We will present our detail data of the study and the perspective of this therapeutic strategy.</description><subject>Alzheimer's disease</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Bone marrow</subject><subject>Cytokines</subject><subject>Drug dosages</subject><subject>Enzymes</subject><subject>Gene therapy</subject><subject>Herpes viruses</subject><subject>Internal medicine</subject><subject>Ischemia</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Nervous system</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Oxidative stress</subject><subject>Performance evaluation</subject><subject>Vectors (Biology)</subject><issn>1525-0016</issn><issn>1525-0024</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNo9kc1OwzAQhCMEEqXwBFxW4pzgn8RJjlD1Tyog0dKr5SYbmpLEwXZb-jo8KaFFXHZnR6Odw-d5t5QElFBxvwkOtVtjwAgRAUkClvAzr0cjFvmEsPD8X1Nx6V1Zu-kUjVLR875ZJAJ41jusYLFGo1rcujKDuTPK4fsBCm1garM11idXfyCsDvCoG4QnZYzeH91aVTDAqrKgmhyGX7Asdxom49HxHo1HDMbYoIWFUY0t0MC-dGt4xbYqM-VK3fjTJtN1iw4bB5P50qewxMxpc-1dFKqyePO3-97baLgYTPzZy3g6eJj5GRUx91UiGFEspGHIySrPabjiUcFVmpA4EWEiRCdSJULRTRbTSOVxGq1yIVJWMB7zvnd3-tsa_blF6-RGb03TVUoapywhNE1Jl-KnVGa0tQYL2ZqyVuYgKZG_MORGHmHIXxiSJLKDwX8APYF80Q</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Nonoguchi, Naosuke</creator><creator>Zhao, Ming-Zhu</creator><creator>Ikeda, Naokado</creator><creator>Miki, Yoshihito</creator><creator>Furutama, Daisuke</creator><creator>Kimura, Fumiharu</creator><creator>Dezawa, Mari</creator><creator>Funakoshi, Hiroshi</creator><creator>Coffin, Robert S.</creator><creator>Miyatake, Shin-ichi</creator><creator>Kuroiwa, Toshihiko</creator><general>Elsevier Limited</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20060501</creationdate><title>256. Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector</title><author>Nonoguchi, Naosuke ; Zhao, Ming-Zhu ; Ikeda, Naokado ; Miki, Yoshihito ; Furutama, Daisuke ; Kimura, Fumiharu ; Dezawa, Mari ; Funakoshi, Hiroshi ; Coffin, Robert S. ; Miyatake, Shin-ichi ; Kuroiwa, Toshihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1673-a8620a2414430bdd14b35f3a98078648668079a64679a2715ad795bd6692f2373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Alzheimer's disease</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Bone marrow</topic><topic>Cytokines</topic><topic>Drug dosages</topic><topic>Enzymes</topic><topic>Gene therapy</topic><topic>Herpes viruses</topic><topic>Internal medicine</topic><topic>Ischemia</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Neurosurgery</topic><topic>Oxidative stress</topic><topic>Performance evaluation</topic><topic>Vectors (Biology)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nonoguchi, Naosuke</creatorcontrib><creatorcontrib>Zhao, Ming-Zhu</creatorcontrib><creatorcontrib>Ikeda, Naokado</creatorcontrib><creatorcontrib>Miki, Yoshihito</creatorcontrib><creatorcontrib>Furutama, Daisuke</creatorcontrib><creatorcontrib>Kimura, Fumiharu</creatorcontrib><creatorcontrib>Dezawa, Mari</creatorcontrib><creatorcontrib>Funakoshi, Hiroshi</creatorcontrib><creatorcontrib>Coffin, Robert S.</creatorcontrib><creatorcontrib>Miyatake, Shin-ichi</creatorcontrib><creatorcontrib>Kuroiwa, Toshihiko</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Molecular therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nonoguchi, Naosuke</au><au>Zhao, Ming-Zhu</au><au>Ikeda, Naokado</au><au>Miki, Yoshihito</au><au>Furutama, Daisuke</au><au>Kimura, Fumiharu</au><au>Dezawa, Mari</au><au>Funakoshi, Hiroshi</au><au>Coffin, Robert S.</au><au>Miyatake, Shin-ichi</au><au>Kuroiwa, Toshihiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>256. Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector</atitle><jtitle>Molecular therapy</jtitle><date>2006-05-01</date><risdate>2006</risdate><volume>13</volume><issue>S1</issue><spage>S98</spage><epage>S99</epage><pages>S98-S99</pages><issn>1525-0016</issn><eissn>1525-0024</eissn><abstract>The bone marrow stromal cells (MSCs), including the primitive pluriopotent mesenchymal stem cells (PMSCs) and the multipotent adult progenitor cells (MAPCs), are attractive targets for cell and gene therapy for various central nervous system disorders.Material and method: For gene modification of MSCs, we used a replication-incompetent HSV-1 vector "1764/4-", triple-deletion mutant of the ICP4, ICP34.5, and VP16. This vector has very high ability of gene transduction to MSC, 70-75% at MOI 10 and 95% at MOI 50, and its expression can carry on at least one month at high level. Two kinds of vectors expressing HGF and FGF-2 were prepared for this study. FGF-2 vector contains the signal sequence of Interleukin-2 (IL-2ss) ahead of FGF-2 gene to enhance its extracellular secretion, because native FGF2 gene don't have the excretion signal. Native MSCs, HGF-MSCs, IL2ss+FGF-2-MSCs and PBS were administered directly into the lesioned brain 24 hours after transient middle cerebral artery occlusion (MCAO) of adult Wister rats.Results: At day 14, each gene modified MSC group showed significant improvement in modified neurological severity score (mNSS) and apparent decreasing of infarct volume compared with native MSC or sham-operated group. (p<0.05). HGF and FGF-2 expression in vivo were strongly kept through the experimental period. In HGF modified MSC-treated group, the MAP-2 positive cell% tends to increase and the TUNEL positive cell% decrease in the ischemic boundary zone (IBZ). The transdifferentiation of transplanted MSCs to central nervous system cell phenotypes was also checked. Most of the transdifferentiated phenotype was GFAP- positive, and the Nestin-positive cells were scarcely able to find out in the host brain.Discussion and Conclusion: By using the replication- incompetent HSV-1 vector, MSCs can be efficiently engineered to secrete a series of various cytokines in large quantities and in the long term in vitro and in vivo that could potentially treat the ischemic stroke of the brain. HGF and FGF-2 gene-transferred MSCs, achieved the remarkable amelioration of neurological symptoms and apparent decreasing of infarct volume comparison with native MSCs in rat MCAO model. It would be appeared that the main mechanism of these therapeutic effects is the neuroprotection (anti-apoptotic effect) in IBZ by various abundant cytokines secreted from gene engineered MSCs. We will present our detail data of the study and the perspective of this therapeutic strategy.</abstract><cop>Milwaukee</cop><pub>Elsevier Limited</pub><doi>10.1016/j.ymthe.2006.08.283</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer's disease Antioxidants Apoptosis Bone marrow Cytokines Drug dosages Enzymes Gene therapy Herpes viruses Internal medicine Ischemia Medical schools Medicine Nervous system Neurons Neurosciences Neurosurgery Oxidative stress Performance evaluation Vectors (Biology) |
| title | 256. Novel Therapeutic Strategy for Ischemic Stroke by Bone Marrow Stromal Cells and Ex Vivo HGF and FGF2 Genes Transfer with Replication-Incompetent HSV-1 Vector |
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