Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model
At present, there are no proven pharmacological treatments demonstrated to improve long term functional outcomes following traumatic brain injury(TBI). In the setting of non-penetrating TBI, sterile brain inflammatory responses are associated with the development of cerebral edema, intracranial hype...
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| Veröffentlicht in: | Scientific reports 2017-04, Vol.7 (1), p.46461-46461, Article 46461 |
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| creator | Laskowitz, Daniel T. Wang, Haichen Chen, Tony Lubkin, David T. Cantillana, Viviana Tu, Tian Ming Kernagis, Dawn Zhou, Guanen Macy, Gary Kolls, Bradley J. Dawson, Hana N. |
| description | At present, there are no proven pharmacological treatments demonstrated to improve long term functional outcomes following traumatic brain injury(TBI). In the setting of non-penetrating TBI, sterile brain inflammatory responses are associated with the development of cerebral edema, intracranial hypertension, and secondary neuronal injury. There is increasing evidence that endogenous apolipoprotein E(apoE) modifies the neuroinflammatory response through its role in downregulating glial activation, however, the intact apoE holoprotein does not cross the blood-brain barrier due to its size. To address this limitation, we developed a small 5 amino acid apoE mimetic peptide(CN-105) that mimics the polar face of the apoE helical domain involved in receptor interactions. The goal of this study was to investigate the therapeutic potential of CN-105 in a murine model of closed head injury. Treatment with CN-105 was associated with a durable improvement in functional outcomes as assessed by Rotarod and Morris Water Maze and a reduction in positive Fluoro-Jade B stained injured neurons and microglial activation. Administration of CN-105 was also associated with reduction in mRNA expression of a subset of inflammatory and immune-related genes. |
| doi_str_mv | 10.1038/srep46461 |
| format | Article |
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In the setting of non-penetrating TBI, sterile brain inflammatory responses are associated with the development of cerebral edema, intracranial hypertension, and secondary neuronal injury. There is increasing evidence that endogenous apolipoprotein E(apoE) modifies the neuroinflammatory response through its role in downregulating glial activation, however, the intact apoE holoprotein does not cross the blood-brain barrier due to its size. To address this limitation, we developed a small 5 amino acid apoE mimetic peptide(CN-105) that mimics the polar face of the apoE helical domain involved in receptor interactions. The goal of this study was to investigate the therapeutic potential of CN-105 in a murine model of closed head injury. Treatment with CN-105 was associated with a durable improvement in functional outcomes as assessed by Rotarod and Morris Water Maze and a reduction in positive Fluoro-Jade B stained injured neurons and microglial activation. Administration of CN-105 was also associated with reduction in mRNA expression of a subset of inflammatory and immune-related genes.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep46461</identifier><identifier>PMID: 28429734</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/21 ; 38 ; 38/61 ; 59 ; 631/378/340 ; 64/60 ; 692/617/375/1345 ; 82/51 ; 96/63 ; Amino acids ; Animal models ; Animals ; Apolipoprotein E ; Apolipoproteins E - pharmacology ; Apolipoproteins E - therapeutic use ; Blood-brain barrier ; Brain Injuries, Traumatic - drug therapy ; Drug therapy ; Edema ; Gene expression ; Head injuries ; Hippocampus - drug effects ; Humanities and Social Sciences ; Hypertension ; Inflammation ; Inflammation - drug therapy ; Mice ; Models, Animal ; multidisciplinary ; Neuronal-glial interactions ; Neurons - drug effects ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Peptide Fragments - pharmacology ; Peptide Fragments - therapeutic use ; Recovery of Function - drug effects ; Science ; Traumatic brain injury</subject><ispartof>Scientific reports, 2017-04, Vol.7 (1), p.46461-46461, Article 46461</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Apr 2017</rights><rights>Copyright © 2017, The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-36ab1bc58f9f9ca1ce738ad0c7989a539a4bb34c67af13aa7707fc7978fbb6633</citedby><cites>FETCH-LOGICAL-c438t-36ab1bc58f9f9ca1ce738ad0c7989a539a4bb34c67af13aa7707fc7978fbb6633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399447/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399447/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,27931,27932,41127,42196,51583,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28429734$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Laskowitz, Daniel T.</creatorcontrib><creatorcontrib>Wang, Haichen</creatorcontrib><creatorcontrib>Chen, Tony</creatorcontrib><creatorcontrib>Lubkin, David T.</creatorcontrib><creatorcontrib>Cantillana, Viviana</creatorcontrib><creatorcontrib>Tu, Tian Ming</creatorcontrib><creatorcontrib>Kernagis, Dawn</creatorcontrib><creatorcontrib>Zhou, Guanen</creatorcontrib><creatorcontrib>Macy, Gary</creatorcontrib><creatorcontrib>Kolls, Bradley J.</creatorcontrib><creatorcontrib>Dawson, Hana N.</creatorcontrib><title>Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>At present, there are no proven pharmacological treatments demonstrated to improve long term functional outcomes following traumatic brain injury(TBI). In the setting of non-penetrating TBI, sterile brain inflammatory responses are associated with the development of cerebral edema, intracranial hypertension, and secondary neuronal injury. There is increasing evidence that endogenous apolipoprotein E(apoE) modifies the neuroinflammatory response through its role in downregulating glial activation, however, the intact apoE holoprotein does not cross the blood-brain barrier due to its size. To address this limitation, we developed a small 5 amino acid apoE mimetic peptide(CN-105) that mimics the polar face of the apoE helical domain involved in receptor interactions. The goal of this study was to investigate the therapeutic potential of CN-105 in a murine model of closed head injury. Treatment with CN-105 was associated with a durable improvement in functional outcomes as assessed by Rotarod and Morris Water Maze and a reduction in positive Fluoro-Jade B stained injured neurons and microglial activation. Administration of CN-105 was also associated with reduction in mRNA expression of a subset of inflammatory and immune-related genes.</description><subject>13</subject><subject>13/21</subject><subject>38</subject><subject>38/61</subject><subject>59</subject><subject>631/378/340</subject><subject>64/60</subject><subject>692/617/375/1345</subject><subject>82/51</subject><subject>96/63</subject><subject>Amino acids</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins E - pharmacology</subject><subject>Apolipoproteins E - therapeutic use</subject><subject>Blood-brain barrier</subject><subject>Brain Injuries, Traumatic - drug therapy</subject><subject>Drug therapy</subject><subject>Edema</subject><subject>Gene expression</subject><subject>Head injuries</subject><subject>Hippocampus - drug effects</subject><subject>Humanities and Social Sciences</subject><subject>Hypertension</subject><subject>Inflammation</subject><subject>Inflammation - 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pharmacology</topic><topic>Apolipoproteins E - therapeutic use</topic><topic>Blood-brain barrier</topic><topic>Brain Injuries, Traumatic - drug therapy</topic><topic>Drug therapy</topic><topic>Edema</topic><topic>Gene expression</topic><topic>Head injuries</topic><topic>Hippocampus - drug effects</topic><topic>Humanities and Social Sciences</topic><topic>Hypertension</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Mice</topic><topic>Models, Animal</topic><topic>multidisciplinary</topic><topic>Neuronal-glial interactions</topic><topic>Neurons - drug effects</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptide Fragments - therapeutic use</topic><topic>Recovery of Function - drug effects</topic><topic>Science</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Laskowitz, Daniel T.</creatorcontrib><creatorcontrib>Wang, Haichen</creatorcontrib><creatorcontrib>Chen, Tony</creatorcontrib><creatorcontrib>Lubkin, David T.</creatorcontrib><creatorcontrib>Cantillana, Viviana</creatorcontrib><creatorcontrib>Tu, Tian Ming</creatorcontrib><creatorcontrib>Kernagis, Dawn</creatorcontrib><creatorcontrib>Zhou, Guanen</creatorcontrib><creatorcontrib>Macy, Gary</creatorcontrib><creatorcontrib>Kolls, Bradley J.</creatorcontrib><creatorcontrib>Dawson, Hana N.</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science 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>Science Database</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Laskowitz, Daniel T.</au><au>Wang, Haichen</au><au>Chen, Tony</au><au>Lubkin, David T.</au><au>Cantillana, Viviana</au><au>Tu, Tian Ming</au><au>Kernagis, Dawn</au><au>Zhou, Guanen</au><au>Macy, Gary</au><au>Kolls, Bradley J.</au><au>Dawson, Hana N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-04-21</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>46461</spage><epage>46461</epage><pages>46461-46461</pages><artnum>46461</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>At present, there are no proven pharmacological treatments demonstrated to improve long term functional outcomes following traumatic brain injury(TBI). In the setting of non-penetrating TBI, sterile brain inflammatory responses are associated with the development of cerebral edema, intracranial hypertension, and secondary neuronal injury. There is increasing evidence that endogenous apolipoprotein E(apoE) modifies the neuroinflammatory response through its role in downregulating glial activation, however, the intact apoE holoprotein does not cross the blood-brain barrier due to its size. To address this limitation, we developed a small 5 amino acid apoE mimetic peptide(CN-105) that mimics the polar face of the apoE helical domain involved in receptor interactions. The goal of this study was to investigate the therapeutic potential of CN-105 in a murine model of closed head injury. Treatment with CN-105 was associated with a durable improvement in functional outcomes as assessed by Rotarod and Morris Water Maze and a reduction in positive Fluoro-Jade B stained injured neurons and microglial activation. Administration of CN-105 was also associated with reduction in mRNA expression of a subset of inflammatory and immune-related genes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28429734</pmid><doi>10.1038/srep46461</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/21 38 38/61 59 631/378/340 64/60 692/617/375/1345 82/51 96/63 Amino acids Animal models Animals Apolipoprotein E Apolipoproteins E - pharmacology Apolipoproteins E - therapeutic use Blood-brain barrier Brain Injuries, Traumatic - drug therapy Drug therapy Edema Gene expression Head injuries Hippocampus - drug effects Humanities and Social Sciences Hypertension Inflammation Inflammation - drug therapy Mice Models, Animal multidisciplinary Neuronal-glial interactions Neurons - drug effects Neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Peptide Fragments - pharmacology Peptide Fragments - therapeutic use Recovery of Function - drug effects Science Traumatic brain injury |
| title | Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model |
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