Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-maste...
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| Veröffentlicht in: | Molecular neurobiology 2018-04, Vol.55 (4), p.2763-2779 |
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| creator | El Amki, Mohamad Dubois, Martine Lefevre-Scelles, Antoine Magne, Nicolas Roussel, Mélanie Clavier, Thomas Guichet, Pierre-Olivier Gérardin, Emmanuel Compère, Vincent Castel, Hélène |
| description | Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10 days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice. |
| doi_str_mv | 10.1007/s12035-017-0514-6 |
| format | Article |
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Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10 days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0514-6</identifier><identifier>PMID: 28455691</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aneurysms ; Animal models ; Animals ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Body Weight ; Brain - blood supply ; Brain - pathology ; Brain injury ; Caspase 3 - metabolism ; Cell Biology ; Cerebral Arteries - pathology ; Cerebral Cortex - pathology ; Cognitive ability ; Cognitive science ; Complications ; Disease Models, Animal ; Hemorrhage ; Injections ; Mice ; Mice, Inbred C57BL ; Morbidity ; Neurobiology ; Neurological diseases ; Neurology ; Neuroscience ; Neurosciences ; Sensorimotor Cortex - pathology ; Sensorimotor system ; Stroke ; Subarachnoid hemorrhage ; Subarachnoid Hemorrhage - cerebrospinal fluid ; Subarachnoid Hemorrhage - complications ; Thrombosis - cerebrospinal fluid ; Thrombosis - etiology ; Thrombosis - pathology ; Transgenic mice ; Vasoconstriction ; Vasospasm, Intracranial - cerebrospinal fluid ; Vasospasm, Intracranial - etiology ; Vasospasm, Intracranial - pathology</subject><ispartof>Molecular neurobiology, 2018-04, Vol.55 (4), p.2763-2779</ispartof><rights>Springer Science+Business Media New York 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-b07cc29318be6e28ccab46478df3cf6964e6077e211a4f1f48b374aa938b286d3</citedby><cites>FETCH-LOGICAL-c406t-b07cc29318be6e28ccab46478df3cf6964e6077e211a4f1f48b374aa938b286d3</cites><orcidid>0000-0002-8972-5555 ; 0000-0003-0115-2199</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-017-0514-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0514-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28455691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://normandie-univ.hal.science/hal-02280048$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>El Amki, Mohamad</creatorcontrib><creatorcontrib>Dubois, Martine</creatorcontrib><creatorcontrib>Lefevre-Scelles, Antoine</creatorcontrib><creatorcontrib>Magne, Nicolas</creatorcontrib><creatorcontrib>Roussel, Mélanie</creatorcontrib><creatorcontrib>Clavier, Thomas</creatorcontrib><creatorcontrib>Guichet, Pierre-Olivier</creatorcontrib><creatorcontrib>Gérardin, Emmanuel</creatorcontrib><creatorcontrib>Compère, Vincent</creatorcontrib><creatorcontrib>Castel, Hélène</creatorcontrib><title>Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10 days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice.</description><subject>Aneurysms</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body Weight</subject><subject>Brain - blood supply</subject><subject>Brain - pathology</subject><subject>Brain injury</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Biology</subject><subject>Cerebral Arteries - pathology</subject><subject>Cerebral Cortex - pathology</subject><subject>Cognitive ability</subject><subject>Cognitive science</subject><subject>Complications</subject><subject>Disease Models, Animal</subject><subject>Hemorrhage</subject><subject>Injections</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Morbidity</subject><subject>Neurobiology</subject><subject>Neurological diseases</subject><subject>Neurology</subject><subject>Neuroscience</subject><subject>Neurosciences</subject><subject>Sensorimotor Cortex - 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blood supply</topic><topic>Brain - pathology</topic><topic>Brain injury</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Biology</topic><topic>Cerebral Arteries - pathology</topic><topic>Cerebral Cortex - pathology</topic><topic>Cognitive ability</topic><topic>Cognitive science</topic><topic>Complications</topic><topic>Disease Models, Animal</topic><topic>Hemorrhage</topic><topic>Injections</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Morbidity</topic><topic>Neurobiology</topic><topic>Neurological diseases</topic><topic>Neurology</topic><topic>Neuroscience</topic><topic>Neurosciences</topic><topic>Sensorimotor Cortex - pathology</topic><topic>Sensorimotor system</topic><topic>Stroke</topic><topic>Subarachnoid hemorrhage</topic><topic>Subarachnoid Hemorrhage - cerebrospinal fluid</topic><topic>Subarachnoid Hemorrhage - complications</topic><topic>Thrombosis - cerebrospinal fluid</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - pathology</topic><topic>Transgenic mice</topic><topic>Vasoconstriction</topic><topic>Vasospasm, Intracranial - 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Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El Amki, Mohamad</au><au>Dubois, Martine</au><au>Lefevre-Scelles, Antoine</au><au>Magne, Nicolas</au><au>Roussel, Mélanie</au><au>Clavier, Thomas</au><au>Guichet, Pierre-Olivier</au><au>Gérardin, Emmanuel</au><au>Compère, Vincent</au><au>Castel, Hélène</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>55</volume><issue>4</issue><spage>2763</spage><epage>2779</epage><pages>2763-2779</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality and morbidity. Long-term cognitive and sensorimotor deficits are serious complications following SAH but still not well explained and described in mouse preclinical models. The aim of our study is to characterize a well-mastered SAH murine model and to establish developing pathological mechanisms leading to cognitive and motor deficits, allowing identification of specific targets involved in these long-term troubles. We hereby demonstrate that the double blood injection model of SAH induced long-lasting large cerebral artery vasospasm (CVS), microthrombosis formation and cerebral brain damage including defect in potential paravascular diffusion. These neurobiological alterations appear to be associated with sensorimotor and cognitive dysfunctions mainly detected 10 days after the bleeding episode. In conclusion, this characterized model of SAH in mice, stressing prolonged neurobiological pathological mechanisms and associated sensitivomotor deficits, will constitute a validated preclinical model to better decipher the link between CVS, long-term cerebral apoptosis and cognitive disorders occurring during SAH and to allow investigating novel therapeutic approaches in transgenic mice.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28455691</pmid><doi>10.1007/s12035-017-0514-6</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-8972-5555</orcidid><orcidid>https://orcid.org/0000-0003-0115-2199</orcidid></addata></record> |
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| ispartof | Molecular neurobiology, 2018-04, Vol.55 (4), p.2763-2779 |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Aneurysms Animal models Animals Apoptosis Biomedical and Life Sciences Biomedicine Body Weight Brain - blood supply Brain - pathology Brain injury Caspase 3 - metabolism Cell Biology Cerebral Arteries - pathology Cerebral Cortex - pathology Cognitive ability Cognitive science Complications Disease Models, Animal Hemorrhage Injections Mice Mice, Inbred C57BL Morbidity Neurobiology Neurological diseases Neurology Neuroscience Neurosciences Sensorimotor Cortex - pathology Sensorimotor system Stroke Subarachnoid hemorrhage Subarachnoid Hemorrhage - cerebrospinal fluid Subarachnoid Hemorrhage - complications Thrombosis - cerebrospinal fluid Thrombosis - etiology Thrombosis - pathology Transgenic mice Vasoconstriction Vasospasm, Intracranial - cerebrospinal fluid Vasospasm, Intracranial - etiology Vasospasm, Intracranial - pathology |
| title | Long-Lasting Cerebral Vasospasm, Microthrombosis, Apoptosis and Paravascular Alterations Associated with Neurological Deficits in a Mouse Model of Subarachnoid Hemorrhage |
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