Neurotrophin-3 provides neuroprotection via TrkC receptor dependent pErk5 activation in a rat surgical brain injury model
Surgical brain injury (SBI) which occurs due to the inadvertent injury inflicted to surrounding brain tissue during neurosurgical procedures can potentiate blood brain barrier (BBB) permeability, brain edema and neurological deficits. This study investigated the role of neurotrophin 3 (NT-3) and tro...
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| Veröffentlicht in: | Experimental neurology 2018-09, Vol.307, p.82-89 |
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| creator | Akyol, Onat Sherchan, Prativa Yilmaz, Gokce Reis, Cesar Ho, Wingi Man Wang, Yuechun Huang, Lei Solaroglu, Ihsan Zhang, John H. |
| description | Surgical brain injury (SBI) which occurs due to the inadvertent injury inflicted to surrounding brain tissue during neurosurgical procedures can potentiate blood brain barrier (BBB) permeability, brain edema and neurological deficits. This study investigated the role of neurotrophin 3 (NT-3) and tropomyosin related kinase receptor C (TrkC) against brain edema and neurological deficits in a rat SBI model.
SBI was induced in male Sprague Dawley rats by partial right frontal lobe resection. Temporal expression of endogenous NT-3 and TrkC was evaluated at 6, 12, 24 and 72 h after SBI. SBI rats received recombinant NT-3 which was directly applied to the brain surgical injury site using gelfoam. Brain edema and neurological function was evaluated at 24 and 72 h after SBI. Small interfering RNA (siRNA) for TrkC and Rap1 was administered via intracerebroventricular injection 24 h before SBI. BBB permeability assay and western blot was performed at 24 h after SBI.
Endogenous NT-3 was decreased and TrkC expression increased after SBI. Topical administration of recombinant NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. Recombinant NT-3 administration increased the expression of phosphorylated Rap1 and Erk5. The protective effect of NT-3 was reversed with TrkC siRNA but not Rap1 siRNA.
Topical application of NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. The protective effect of NT-3 was possibly mediated via TrkC dependent activation of Erk5.
[Display omitted]
•Endogenous NT-3 expression decreased after SBI.•TrkC receptor expression increased after SBI.•Topical recombinant NT-3 administration improved SBI outcomes.•NT-3 effects were mediated via Erk5 activation dependent on TrkC receptor. |
| doi_str_mv | 10.1016/j.expneurol.2018.06.002 |
| format | Article |
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SBI was induced in male Sprague Dawley rats by partial right frontal lobe resection. Temporal expression of endogenous NT-3 and TrkC was evaluated at 6, 12, 24 and 72 h after SBI. SBI rats received recombinant NT-3 which was directly applied to the brain surgical injury site using gelfoam. Brain edema and neurological function was evaluated at 24 and 72 h after SBI. Small interfering RNA (siRNA) for TrkC and Rap1 was administered via intracerebroventricular injection 24 h before SBI. BBB permeability assay and western blot was performed at 24 h after SBI.
Endogenous NT-3 was decreased and TrkC expression increased after SBI. Topical administration of recombinant NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. Recombinant NT-3 administration increased the expression of phosphorylated Rap1 and Erk5. The protective effect of NT-3 was reversed with TrkC siRNA but not Rap1 siRNA.
Topical application of NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. The protective effect of NT-3 was possibly mediated via TrkC dependent activation of Erk5.
[Display omitted]
•Endogenous NT-3 expression decreased after SBI.•TrkC receptor expression increased after SBI.•Topical recombinant NT-3 administration improved SBI outcomes.•NT-3 effects were mediated via Erk5 activation dependent on TrkC receptor.</description><identifier>ISSN: 0014-4886</identifier><identifier>EISSN: 1090-2430</identifier><identifier>DOI: 10.1016/j.expneurol.2018.06.002</identifier><identifier>PMID: 29883578</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Administration, Topical ; Animals ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - metabolism ; Brain edema ; Brain Injuries - etiology ; Brain Injuries - metabolism ; Brain Injuries - prevention & control ; Enzyme Activation - drug effects ; Enzyme Activation - physiology ; Extracellular signal related kinase 5 ; Male ; Mitogen-Activated Protein Kinase 7 - metabolism ; Neuroprotection - drug effects ; Neuroprotection - physiology ; Neurosurgical Procedures - adverse effects ; Neurotrophin 3 ; Neurotrophin 3 - administration & dosage ; Rats ; Rats, Sprague-Dawley ; Receptor, trkC - metabolism ; Surgical brain injury ; Tropomyosin related kinase receptor C</subject><ispartof>Experimental neurology, 2018-09, Vol.307, p.82-89</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-471a4946f0cd7fbd9f1a9388b0fbed02ee7f1667540c64a64b6e2899cbf738a73</citedby><cites>FETCH-LOGICAL-c475t-471a4946f0cd7fbd9f1a9388b0fbed02ee7f1667540c64a64b6e2899cbf738a73</cites><orcidid>0000-0002-4319-4285</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.expneurol.2018.06.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29883578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Akyol, Onat</creatorcontrib><creatorcontrib>Sherchan, Prativa</creatorcontrib><creatorcontrib>Yilmaz, Gokce</creatorcontrib><creatorcontrib>Reis, Cesar</creatorcontrib><creatorcontrib>Ho, Wingi Man</creatorcontrib><creatorcontrib>Wang, Yuechun</creatorcontrib><creatorcontrib>Huang, Lei</creatorcontrib><creatorcontrib>Solaroglu, Ihsan</creatorcontrib><creatorcontrib>Zhang, John H.</creatorcontrib><title>Neurotrophin-3 provides neuroprotection via TrkC receptor dependent pErk5 activation in a rat surgical brain injury model</title><title>Experimental neurology</title><addtitle>Exp Neurol</addtitle><description>Surgical brain injury (SBI) which occurs due to the inadvertent injury inflicted to surrounding brain tissue during neurosurgical procedures can potentiate blood brain barrier (BBB) permeability, brain edema and neurological deficits. This study investigated the role of neurotrophin 3 (NT-3) and tropomyosin related kinase receptor C (TrkC) against brain edema and neurological deficits in a rat SBI model.
SBI was induced in male Sprague Dawley rats by partial right frontal lobe resection. Temporal expression of endogenous NT-3 and TrkC was evaluated at 6, 12, 24 and 72 h after SBI. SBI rats received recombinant NT-3 which was directly applied to the brain surgical injury site using gelfoam. Brain edema and neurological function was evaluated at 24 and 72 h after SBI. Small interfering RNA (siRNA) for TrkC and Rap1 was administered via intracerebroventricular injection 24 h before SBI. BBB permeability assay and western blot was performed at 24 h after SBI.
Endogenous NT-3 was decreased and TrkC expression increased after SBI. Topical administration of recombinant NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. Recombinant NT-3 administration increased the expression of phosphorylated Rap1 and Erk5. The protective effect of NT-3 was reversed with TrkC siRNA but not Rap1 siRNA.
Topical application of NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. The protective effect of NT-3 was possibly mediated via TrkC dependent activation of Erk5.
[Display omitted]
•Endogenous NT-3 expression decreased after SBI.•TrkC receptor expression increased after SBI.•Topical recombinant NT-3 administration improved SBI outcomes.•NT-3 effects were mediated via Erk5 activation dependent on TrkC receptor.</description><subject>Administration, Topical</subject><subject>Animals</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Brain edema</subject><subject>Brain Injuries - etiology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - prevention & control</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Activation - physiology</subject><subject>Extracellular signal related kinase 5</subject><subject>Male</subject><subject>Mitogen-Activated Protein Kinase 7 - metabolism</subject><subject>Neuroprotection - drug effects</subject><subject>Neuroprotection - physiology</subject><subject>Neurosurgical Procedures - adverse effects</subject><subject>Neurotrophin 3</subject><subject>Neurotrophin 3 - administration & dosage</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, trkC - metabolism</subject><subject>Surgical brain injury</subject><subject>Tropomyosin related kinase receptor C</subject><issn>0014-4886</issn><issn>1090-2430</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EokvhL4CPXBLGjuPYF6RqVT6kCi7lbDn2pPU2Gwc7idh_T7ZbVnDiZNnzzDsjP4S8Y1AyYPLDrsRf44Bzin3JgakSZAnAn5ENAw0FFxU8JxsAJgqhlLwgr3LeAYAWvHlJLrhWqqobtSGHb8eQKcXxPgxFRccUl-Ax08fw9Tahm0Ic6BIsvU0PW5rQ4TjFRD2OOHgcJjpep4ea2hVc7CMcBmppshPNc7oLzva0TTYc33dzOtB99Ni_Ji8622d883Rekh-frm-3X4qb75-_bq9uCieaeipEw6zQQnbgfNO1XnfM6kqpFroWPXDEpmNSNrUAJ4WVopXIldau7ZpK2aa6JB9PuePc7tG7deFkezOmsLfpYKIN5t_KEO7NXVyMUrqqtV4D3j8FpPhzxjyZfcgO-94OGOdsONRcgaw4rGhzQl2KOSfszmMYmKM4szNnceYozoA0q7i18-3fW577_phagasTgOtfLQGTyS7g4NCH1chkfAz_HfIbx5ay1Q</recordid><startdate>20180901</startdate><enddate>20180901</enddate><creator>Akyol, Onat</creator><creator>Sherchan, Prativa</creator><creator>Yilmaz, Gokce</creator><creator>Reis, Cesar</creator><creator>Ho, Wingi Man</creator><creator>Wang, Yuechun</creator><creator>Huang, Lei</creator><creator>Solaroglu, Ihsan</creator><creator>Zhang, John H.</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4319-4285</orcidid></search><sort><creationdate>20180901</creationdate><title>Neurotrophin-3 provides neuroprotection via TrkC receptor dependent pErk5 activation in a rat surgical brain injury model</title><author>Akyol, Onat ; Sherchan, Prativa ; Yilmaz, Gokce ; Reis, Cesar ; Ho, Wingi Man ; Wang, Yuechun ; Huang, Lei ; Solaroglu, Ihsan ; Zhang, John H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-471a4946f0cd7fbd9f1a9388b0fbed02ee7f1667540c64a64b6e2899cbf738a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Administration, Topical</topic><topic>Animals</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Brain edema</topic><topic>Brain Injuries - etiology</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - prevention & control</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Activation - physiology</topic><topic>Extracellular signal related kinase 5</topic><topic>Male</topic><topic>Mitogen-Activated Protein Kinase 7 - metabolism</topic><topic>Neuroprotection - drug effects</topic><topic>Neuroprotection - physiology</topic><topic>Neurosurgical Procedures - adverse effects</topic><topic>Neurotrophin 3</topic><topic>Neurotrophin 3 - administration & dosage</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, trkC - metabolism</topic><topic>Surgical brain injury</topic><topic>Tropomyosin related kinase receptor C</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Akyol, Onat</creatorcontrib><creatorcontrib>Sherchan, Prativa</creatorcontrib><creatorcontrib>Yilmaz, Gokce</creatorcontrib><creatorcontrib>Reis, Cesar</creatorcontrib><creatorcontrib>Ho, Wingi Man</creatorcontrib><creatorcontrib>Wang, Yuechun</creatorcontrib><creatorcontrib>Huang, Lei</creatorcontrib><creatorcontrib>Solaroglu, Ihsan</creatorcontrib><creatorcontrib>Zhang, John H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Akyol, Onat</au><au>Sherchan, Prativa</au><au>Yilmaz, Gokce</au><au>Reis, Cesar</au><au>Ho, Wingi Man</au><au>Wang, Yuechun</au><au>Huang, Lei</au><au>Solaroglu, Ihsan</au><au>Zhang, John H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neurotrophin-3 provides neuroprotection via TrkC receptor dependent pErk5 activation in a rat surgical brain injury model</atitle><jtitle>Experimental neurology</jtitle><addtitle>Exp Neurol</addtitle><date>2018-09-01</date><risdate>2018</risdate><volume>307</volume><spage>82</spage><epage>89</epage><pages>82-89</pages><issn>0014-4886</issn><eissn>1090-2430</eissn><abstract>Surgical brain injury (SBI) which occurs due to the inadvertent injury inflicted to surrounding brain tissue during neurosurgical procedures can potentiate blood brain barrier (BBB) permeability, brain edema and neurological deficits. This study investigated the role of neurotrophin 3 (NT-3) and tropomyosin related kinase receptor C (TrkC) against brain edema and neurological deficits in a rat SBI model.
SBI was induced in male Sprague Dawley rats by partial right frontal lobe resection. Temporal expression of endogenous NT-3 and TrkC was evaluated at 6, 12, 24 and 72 h after SBI. SBI rats received recombinant NT-3 which was directly applied to the brain surgical injury site using gelfoam. Brain edema and neurological function was evaluated at 24 and 72 h after SBI. Small interfering RNA (siRNA) for TrkC and Rap1 was administered via intracerebroventricular injection 24 h before SBI. BBB permeability assay and western blot was performed at 24 h after SBI.
Endogenous NT-3 was decreased and TrkC expression increased after SBI. Topical administration of recombinant NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. Recombinant NT-3 administration increased the expression of phosphorylated Rap1 and Erk5. The protective effect of NT-3 was reversed with TrkC siRNA but not Rap1 siRNA.
Topical application of NT-3 reduced brain edema, BBB permeability and improved neurological function after SBI. The protective effect of NT-3 was possibly mediated via TrkC dependent activation of Erk5.
[Display omitted]
•Endogenous NT-3 expression decreased after SBI.•TrkC receptor expression increased after SBI.•Topical recombinant NT-3 administration improved SBI outcomes.•NT-3 effects were mediated via Erk5 activation dependent on TrkC receptor.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29883578</pmid><doi>10.1016/j.expneurol.2018.06.002</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-4319-4285</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Administration, Topical Animals Blood-Brain Barrier - drug effects Blood-Brain Barrier - metabolism Brain edema Brain Injuries - etiology Brain Injuries - metabolism Brain Injuries - prevention & control Enzyme Activation - drug effects Enzyme Activation - physiology Extracellular signal related kinase 5 Male Mitogen-Activated Protein Kinase 7 - metabolism Neuroprotection - drug effects Neuroprotection - physiology Neurosurgical Procedures - adverse effects Neurotrophin 3 Neurotrophin 3 - administration & dosage Rats Rats, Sprague-Dawley Receptor, trkC - metabolism Surgical brain injury Tropomyosin related kinase receptor C |
| title | Neurotrophin-3 provides neuroprotection via TrkC receptor dependent pErk5 activation in a rat surgical brain injury model |
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