White matter activated glial cells produce BDNF in a stroke model of monkeys
Lacunar-type stroke accounts for approximately a quarter of all ischemic strokes, and is the most common cause of vascular dementia. Despite its importance, there are few specific treatments for lacunar stroke, probably due largely to a lack of animal models. In this study, we developed a stroke mod...
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| Veröffentlicht in: | Neuroscience research 2009-09, Vol.65 (1), p.71-78 |
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| creator | Sato, Yuki Chin, Yo Kato, Tomomasa Tanaka, Yuichi Tozuka, Yusuke Mase, Mitsuhito Ageyama, Naohide Ono, Fumiko Terao, Keiji Yoshikawa, Yasuhiro Hisatsune, Tatsuhiro |
| description | Lacunar-type stroke accounts for approximately a quarter of all ischemic strokes, and is the most common cause of vascular dementia. Despite its importance, there are few specific treatments for lacunar stroke, probably due largely to a lack of animal models. In this study, we developed a stroke model in a higher primate, the Macaque monkey. This was achieved by occluding the deep subcortical penetrating arteries with agarose spheres of mean diameters around 50
μm, and the appropriateness of this model as a lacunar-type stroke was verified by MRI. We observed widespread gliosis in the ipsilateral white matter (WM) of the stroke monkey. We also analyzed the expression of neurotrophins in the activated glial cells, and found that their expression of BDNF was stimulated in the affected WM following ischemic injury. Our results support the idea that WM glial cells play an active role in protecting and promoting the regeneration of nerve fibers in the affected WM of the ischemic brain, by producing BDNF. These findings may be useful for the development of new therapeutic strategies aimed at preventing or treating stroke. |
| doi_str_mv | 10.1016/j.neures.2009.05.010 |
| format | Article |
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μm, and the appropriateness of this model as a lacunar-type stroke was verified by MRI. We observed widespread gliosis in the ipsilateral white matter (WM) of the stroke monkey. We also analyzed the expression of neurotrophins in the activated glial cells, and found that their expression of BDNF was stimulated in the affected WM following ischemic injury. Our results support the idea that WM glial cells play an active role in protecting and promoting the regeneration of nerve fibers in the affected WM of the ischemic brain, by producing BDNF. These findings may be useful for the development of new therapeutic strategies aimed at preventing or treating stroke.</description><identifier>ISSN: 0168-0102</identifier><identifier>EISSN: 1872-8111</identifier><identifier>DOI: 10.1016/j.neures.2009.05.010</identifier><identifier>PMID: 19501123</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; Astrocytes - metabolism ; BDNF ; Brain Infarction - metabolism ; Brain Infarction - physiopathology ; Brain-Derived Neurotrophic Factor - metabolism ; Disease Models, Animal ; Fluorescent Antibody Technique ; Glial Fibrillary Acidic Protein - metabolism ; Gliosis - metabolism ; Gliosis - physiopathology ; Internal Capsule - metabolism ; Internal Capsule - physiopathology ; Ischemic injuries ; Macaca ; Macaca fascicularis ; Magnetic Resonance Imaging ; Male ; Primates ; Reactive astrocytes ; Stroke - metabolism ; Stroke - physiopathology ; White matter</subject><ispartof>Neuroscience research, 2009-09, Vol.65 (1), p.71-78</ispartof><rights>2009 Elsevier Ireland Ltd and the Japan Neuroscience Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-58539a35acd2c2e1d26662b01754cac8fa1ee973bfb3cb7c36a5403d01378d2b3</citedby><cites>FETCH-LOGICAL-c510t-58539a35acd2c2e1d26662b01754cac8fa1ee973bfb3cb7c36a5403d01378d2b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S016801020900176X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19501123$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sato, Yuki</creatorcontrib><creatorcontrib>Chin, Yo</creatorcontrib><creatorcontrib>Kato, Tomomasa</creatorcontrib><creatorcontrib>Tanaka, Yuichi</creatorcontrib><creatorcontrib>Tozuka, Yusuke</creatorcontrib><creatorcontrib>Mase, Mitsuhito</creatorcontrib><creatorcontrib>Ageyama, Naohide</creatorcontrib><creatorcontrib>Ono, Fumiko</creatorcontrib><creatorcontrib>Terao, Keiji</creatorcontrib><creatorcontrib>Yoshikawa, Yasuhiro</creatorcontrib><creatorcontrib>Hisatsune, Tatsuhiro</creatorcontrib><title>White matter activated glial cells produce BDNF in a stroke model of monkeys</title><title>Neuroscience research</title><addtitle>Neurosci Res</addtitle><description>Lacunar-type stroke accounts for approximately a quarter of all ischemic strokes, and is the most common cause of vascular dementia. Despite its importance, there are few specific treatments for lacunar stroke, probably due largely to a lack of animal models. In this study, we developed a stroke model in a higher primate, the Macaque monkey. This was achieved by occluding the deep subcortical penetrating arteries with agarose spheres of mean diameters around 50
μm, and the appropriateness of this model as a lacunar-type stroke was verified by MRI. We observed widespread gliosis in the ipsilateral white matter (WM) of the stroke monkey. We also analyzed the expression of neurotrophins in the activated glial cells, and found that their expression of BDNF was stimulated in the affected WM following ischemic injury. Our results support the idea that WM glial cells play an active role in protecting and promoting the regeneration of nerve fibers in the affected WM of the ischemic brain, by producing BDNF. These findings may be useful for the development of new therapeutic strategies aimed at preventing or treating stroke.</description><subject>Animals</subject><subject>Astrocytes - metabolism</subject><subject>BDNF</subject><subject>Brain Infarction - metabolism</subject><subject>Brain Infarction - physiopathology</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Disease Models, Animal</subject><subject>Fluorescent Antibody Technique</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Gliosis - metabolism</subject><subject>Gliosis - physiopathology</subject><subject>Internal Capsule - metabolism</subject><subject>Internal Capsule - physiopathology</subject><subject>Ischemic injuries</subject><subject>Macaca</subject><subject>Macaca fascicularis</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Primates</subject><subject>Reactive astrocytes</subject><subject>Stroke - metabolism</subject><subject>Stroke - physiopathology</subject><subject>White matter</subject><issn>0168-0102</issn><issn>1872-8111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQhi1ERbcL_wAhn7glnbHjfFwqlX4ircoFxNFy7Al4m02K7VTqv69XuxI3OM1o9Lwzo4exjwglAtbn23KiJVAsBUBXgioB4Q1bYduIokXEt2yVsbbIY3HKzmLcAoDsKvmOnWKnAFHIFdv8_O0T8Z1JiQI3Nvlnk8jxX6M3I7c0jpE_hdktlviX64db7idueExhfsyp2dHI5yE30yO9xPfsZDBjpA_HumY_bm--X90Xm293X68uN4VVCKlQrZKdkcpYJ6wgdKKua9EDNqqyxraDQaKukf3QS9s3VtZGVSAdoGxaJ3q5Zp8Pe_NnfxaKSe983P9qJpqXqOsm36lF819QgKiwzk7WrDqANswxBhr0U_A7E140gt7r1lt90K33ujUonb3m2Kfj_qXfkfsbOvrNwMUBoKzj2VPQ0XqaLDkfyCbtZv_vC69QmpHa</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Sato, Yuki</creator><creator>Chin, Yo</creator><creator>Kato, Tomomasa</creator><creator>Tanaka, Yuichi</creator><creator>Tozuka, Yusuke</creator><creator>Mase, Mitsuhito</creator><creator>Ageyama, Naohide</creator><creator>Ono, Fumiko</creator><creator>Terao, Keiji</creator><creator>Yoshikawa, Yasuhiro</creator><creator>Hisatsune, Tatsuhiro</creator><general>Elsevier Ireland Ltd</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20090901</creationdate><title>White matter activated glial cells produce BDNF in a stroke model of monkeys</title><author>Sato, Yuki ; Chin, Yo ; Kato, Tomomasa ; Tanaka, Yuichi ; Tozuka, Yusuke ; Mase, Mitsuhito ; Ageyama, Naohide ; Ono, Fumiko ; Terao, Keiji ; Yoshikawa, Yasuhiro ; Hisatsune, Tatsuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-58539a35acd2c2e1d26662b01754cac8fa1ee973bfb3cb7c36a5403d01378d2b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Astrocytes - metabolism</topic><topic>BDNF</topic><topic>Brain Infarction - metabolism</topic><topic>Brain Infarction - physiopathology</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Disease Models, Animal</topic><topic>Fluorescent Antibody Technique</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Gliosis - metabolism</topic><topic>Gliosis - physiopathology</topic><topic>Internal Capsule - metabolism</topic><topic>Internal Capsule - physiopathology</topic><topic>Ischemic injuries</topic><topic>Macaca</topic><topic>Macaca fascicularis</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Primates</topic><topic>Reactive astrocytes</topic><topic>Stroke - metabolism</topic><topic>Stroke - physiopathology</topic><topic>White matter</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sato, Yuki</creatorcontrib><creatorcontrib>Chin, Yo</creatorcontrib><creatorcontrib>Kato, Tomomasa</creatorcontrib><creatorcontrib>Tanaka, Yuichi</creatorcontrib><creatorcontrib>Tozuka, Yusuke</creatorcontrib><creatorcontrib>Mase, Mitsuhito</creatorcontrib><creatorcontrib>Ageyama, Naohide</creatorcontrib><creatorcontrib>Ono, Fumiko</creatorcontrib><creatorcontrib>Terao, Keiji</creatorcontrib><creatorcontrib>Yoshikawa, Yasuhiro</creatorcontrib><creatorcontrib>Hisatsune, Tatsuhiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sato, Yuki</au><au>Chin, Yo</au><au>Kato, Tomomasa</au><au>Tanaka, Yuichi</au><au>Tozuka, Yusuke</au><au>Mase, Mitsuhito</au><au>Ageyama, Naohide</au><au>Ono, Fumiko</au><au>Terao, Keiji</au><au>Yoshikawa, Yasuhiro</au><au>Hisatsune, Tatsuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>White matter activated glial cells produce BDNF in a stroke model of monkeys</atitle><jtitle>Neuroscience research</jtitle><addtitle>Neurosci Res</addtitle><date>2009-09-01</date><risdate>2009</risdate><volume>65</volume><issue>1</issue><spage>71</spage><epage>78</epage><pages>71-78</pages><issn>0168-0102</issn><eissn>1872-8111</eissn><abstract>Lacunar-type stroke accounts for approximately a quarter of all ischemic strokes, and is the most common cause of vascular dementia. Despite its importance, there are few specific treatments for lacunar stroke, probably due largely to a lack of animal models. In this study, we developed a stroke model in a higher primate, the Macaque monkey. This was achieved by occluding the deep subcortical penetrating arteries with agarose spheres of mean diameters around 50
μm, and the appropriateness of this model as a lacunar-type stroke was verified by MRI. We observed widespread gliosis in the ipsilateral white matter (WM) of the stroke monkey. We also analyzed the expression of neurotrophins in the activated glial cells, and found that their expression of BDNF was stimulated in the affected WM following ischemic injury. Our results support the idea that WM glial cells play an active role in protecting and promoting the regeneration of nerve fibers in the affected WM of the ischemic brain, by producing BDNF. These findings may be useful for the development of new therapeutic strategies aimed at preventing or treating stroke.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>19501123</pmid><doi>10.1016/j.neures.2009.05.010</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Astrocytes - metabolism BDNF Brain Infarction - metabolism Brain Infarction - physiopathology Brain-Derived Neurotrophic Factor - metabolism Disease Models, Animal Fluorescent Antibody Technique Glial Fibrillary Acidic Protein - metabolism Gliosis - metabolism Gliosis - physiopathology Internal Capsule - metabolism Internal Capsule - physiopathology Ischemic injuries Macaca Macaca fascicularis Magnetic Resonance Imaging Male Primates Reactive astrocytes Stroke - metabolism Stroke - physiopathology White matter |
| title | White matter activated glial cells produce BDNF in a stroke model of monkeys |
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