Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury
Many cellular responses to Ca 2+ signals are mediated by Ca 2+ /calmodulin-dependent enzymes, among which is the Ca 2+ /calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β...
Gespeichert in:
| Veröffentlicht in: | Journal of molecular neuroscience 2012-03, Vol.46 (3), p.631-643 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 643 |
|---|---|
| container_issue | 3 |
| container_start_page | 631 |
| container_title | Journal of molecular neuroscience |
| container_volume | 46 |
| creator | Zhang, Mingyang Shan, Haiyan Gu, Zhenyong Wang, Donglin Wang, Tao Wang, Zhiwei Tao, Luyang |
| description | Many cellular responses to Ca
2+
signals are mediated by Ca
2+
/calmodulin-dependent enzymes, among which is the Ca
2+
/calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β, γ, and δ. This study aims to investigate changes of CaMKIIδ after traumatic brain injury and its possible role. Rat traumatic brain injury (TBI) model was established by controlled cortical injury system. In the present study, we mainly investigated the expression and cellular localization of CaMKIIδ after traumatic brain injury. Western blot analysis revealed that CaMKIIδ was present in normal rat brain cortex. It gradually increased, reached a peak at the third day after TBI, and then decreased. Importantly, more CaMKIIδ was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3.Importantly, immunohistochemistry analysis revealed that injury-induced expression of CaMKIIδ was colabeled by caspase-3 (apoptosis cells marker). Moreover, pretreatment with the CaMKII inhibitor (KN62) reduced the injury-induced activation of caspase-3. Noticeably, the CaMKII inhibitor KN-62 could reduce TBI-induced cell injury assessed with lesion volume and attenuate behavioral outcome evaluated by motor test. These data suggested that CaMKIIδ may be implicated in the apoptosis of neuron and the recovery of neurological outcomes. However, the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of CaMKIIδ after brain injury. |
| doi_str_mv | 10.1007/s12031-011-9651-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_926884107</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>926884107</sourcerecordid><originalsourceid>FETCH-LOGICAL-c402t-50cdb02c87763800a62985a39edcc0ac5cc5e31662f383c6f93167f11171e0f83</originalsourceid><addsrcrecordid>eNqNkU2L1EAQhhtxccfVH-BFGi-e4lZ1kk7nqLOrhl1Y0fEcejoVyZB0Yn-A8dfbw6wKgrCnounnfYviYewFwhsEqC49CsgxA8SsliVm6yO2wbKsM0QpH7MNqLrMlKzlOXvq_QFAYIHqCTsXAgpVC9iwn401jrSnjl__WBx5P8yWzz3f6tEMcbpMc5q7OA42u6KFbEc28E9uDjRYfjPYFOW7dSHeNPxL3Ec7BH5FY9Bc94Ec_6wD3zkdJx0Gw985nWKNPUS3PmNnvR49Pb-fF-zr--vd9mN2e_eh2b69zUwBImQlmG4PwqiqkrkC0FLUqtR5TZ0xoE1pTEl5Olj0ucqN7Ov0qHpErJCgV_kFe33qXdz8PZIP7TR4Q-OoLc3Rt7WQShUI1QNIUUlMbCJf_UMe5uhsOiNBWFZVIY6L8QQZN3vvqG8XN0zarS1CexTYngS2SWB7FNiuKfPyvjjuJ-r-JH4bS4A4AT592W_k_m7-f-svXrKlrA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>921577428</pqid></control><display><type>article</type><title>Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Zhang, Mingyang ; Shan, Haiyan ; Gu, Zhenyong ; Wang, Donglin ; Wang, Tao ; Wang, Zhiwei ; Tao, Luyang</creator><creatorcontrib>Zhang, Mingyang ; Shan, Haiyan ; Gu, Zhenyong ; Wang, Donglin ; Wang, Tao ; Wang, Zhiwei ; Tao, Luyang</creatorcontrib><description>Many cellular responses to Ca
2+
signals are mediated by Ca
2+
/calmodulin-dependent enzymes, among which is the Ca
2+
/calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β, γ, and δ. This study aims to investigate changes of CaMKIIδ after traumatic brain injury and its possible role. Rat traumatic brain injury (TBI) model was established by controlled cortical injury system. In the present study, we mainly investigated the expression and cellular localization of CaMKIIδ after traumatic brain injury. Western blot analysis revealed that CaMKIIδ was present in normal rat brain cortex. It gradually increased, reached a peak at the third day after TBI, and then decreased. Importantly, more CaMKIIδ was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3.Importantly, immunohistochemistry analysis revealed that injury-induced expression of CaMKIIδ was colabeled by caspase-3 (apoptosis cells marker). Moreover, pretreatment with the CaMKII inhibitor (KN62) reduced the injury-induced activation of caspase-3. Noticeably, the CaMKII inhibitor KN-62 could reduce TBI-induced cell injury assessed with lesion volume and attenuate behavioral outcome evaluated by motor test. These data suggested that CaMKIIδ may be implicated in the apoptosis of neuron and the recovery of neurological outcomes. However, the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of CaMKIIδ after brain injury.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-011-9651-y</identifier><identifier>PMID: 22048920</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives ; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology ; Animals ; Apoptosis ; Apoptosis - physiology ; Biomedical and Life Sciences ; Biomedicine ; Brain Injuries - genetics ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Ca super(2+)/calmodulin-dependent protein kinase II ; Calcium ; Calcium Signaling - physiology ; Calcium signalling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - biosynthesis ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics ; Caspase 3 - metabolism ; Caspase-3 ; Cell Biology ; Cell injury ; Cortex ; Data processing ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Enzymes ; Forensic sciences ; Gene expression ; Immunohistochemistry ; Kinases ; Laboratory animals ; Male ; Nerve Degeneration - metabolism ; Nerve Degeneration - pathology ; Nervous system ; Neurochemistry ; Neurology ; Neurons ; Neurons - metabolism ; Neurons - pathology ; Neurosciences ; Proteins ; Proteomics ; Rats ; Rats, Sprague-Dawley ; Recovery of Function - physiology ; Surgery ; Traumatic brain injury ; Up-Regulation - physiology ; Western blotting</subject><ispartof>Journal of molecular neuroscience, 2012-03, Vol.46 (3), p.631-643</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><rights>Springer Science+Business Media, LLC 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-50cdb02c87763800a62985a39edcc0ac5cc5e31662f383c6f93167f11171e0f83</citedby><cites>FETCH-LOGICAL-c402t-50cdb02c87763800a62985a39edcc0ac5cc5e31662f383c6f93167f11171e0f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-011-9651-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-011-9651-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22048920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Mingyang</creatorcontrib><creatorcontrib>Shan, Haiyan</creatorcontrib><creatorcontrib>Gu, Zhenyong</creatorcontrib><creatorcontrib>Wang, Donglin</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Wang, Zhiwei</creatorcontrib><creatorcontrib>Tao, Luyang</creatorcontrib><title>Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Many cellular responses to Ca
2+
signals are mediated by Ca
2+
/calmodulin-dependent enzymes, among which is the Ca
2+
/calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β, γ, and δ. This study aims to investigate changes of CaMKIIδ after traumatic brain injury and its possible role. Rat traumatic brain injury (TBI) model was established by controlled cortical injury system. In the present study, we mainly investigated the expression and cellular localization of CaMKIIδ after traumatic brain injury. Western blot analysis revealed that CaMKIIδ was present in normal rat brain cortex. It gradually increased, reached a peak at the third day after TBI, and then decreased. Importantly, more CaMKIIδ was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3.Importantly, immunohistochemistry analysis revealed that injury-induced expression of CaMKIIδ was colabeled by caspase-3 (apoptosis cells marker). Moreover, pretreatment with the CaMKII inhibitor (KN62) reduced the injury-induced activation of caspase-3. Noticeably, the CaMKII inhibitor KN-62 could reduce TBI-induced cell injury assessed with lesion volume and attenuate behavioral outcome evaluated by motor test. These data suggested that CaMKIIδ may be implicated in the apoptosis of neuron and the recovery of neurological outcomes. However, the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of CaMKIIδ after brain injury.</description><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</subject><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain Injuries - genetics</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Ca super(2+)/calmodulin-dependent protein kinase II</subject><subject>Calcium</subject><subject>Calcium Signaling - physiology</subject><subject>Calcium signalling</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - biosynthesis</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Cell injury</subject><subject>Cortex</subject><subject>Data processing</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzymes</subject><subject>Forensic sciences</subject><subject>Gene expression</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - pathology</subject><subject>Nervous system</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurosciences</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Recovery of Function - physiology</subject><subject>Surgery</subject><subject>Traumatic brain injury</subject><subject>Up-Regulation - physiology</subject><subject>Western blotting</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkU2L1EAQhhtxccfVH-BFGi-e4lZ1kk7nqLOrhl1Y0fEcejoVyZB0Yn-A8dfbw6wKgrCnounnfYviYewFwhsEqC49CsgxA8SsliVm6yO2wbKsM0QpH7MNqLrMlKzlOXvq_QFAYIHqCTsXAgpVC9iwn401jrSnjl__WBx5P8yWzz3f6tEMcbpMc5q7OA42u6KFbEc28E9uDjRYfjPYFOW7dSHeNPxL3Ec7BH5FY9Bc94Ec_6wD3zkdJx0Gw985nWKNPUS3PmNnvR49Pb-fF-zr--vd9mN2e_eh2b69zUwBImQlmG4PwqiqkrkC0FLUqtR5TZ0xoE1pTEl5Olj0ucqN7Ov0qHpErJCgV_kFe33qXdz8PZIP7TR4Q-OoLc3Rt7WQShUI1QNIUUlMbCJf_UMe5uhsOiNBWFZVIY6L8QQZN3vvqG8XN0zarS1CexTYngS2SWB7FNiuKfPyvjjuJ-r-JH4bS4A4AT592W_k_m7-f-svXrKlrA</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Zhang, Mingyang</creator><creator>Shan, Haiyan</creator><creator>Gu, Zhenyong</creator><creator>Wang, Donglin</creator><creator>Wang, Tao</creator><creator>Wang, Zhiwei</creator><creator>Tao, Luyang</creator><general>Humana Press Inc</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120301</creationdate><title>Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury</title><author>Zhang, Mingyang ; Shan, Haiyan ; Gu, Zhenyong ; Wang, Donglin ; Wang, Tao ; Wang, Zhiwei ; Tao, Luyang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-50cdb02c87763800a62985a39edcc0ac5cc5e31662f383c6f93167f11171e0f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</topic><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain Injuries - genetics</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - pathology</topic><topic>Ca super(2+)/calmodulin-dependent protein kinase II</topic><topic>Calcium</topic><topic>Calcium Signaling - physiology</topic><topic>Calcium signalling</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - biosynthesis</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell Biology</topic><topic>Cell injury</topic><topic>Cortex</topic><topic>Data processing</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Enzymes</topic><topic>Forensic sciences</topic><topic>Gene expression</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Nerve Degeneration - metabolism</topic><topic>Nerve Degeneration - pathology</topic><topic>Nervous system</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neurosciences</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Recovery of Function - physiology</topic><topic>Surgery</topic><topic>Traumatic brain injury</topic><topic>Up-Regulation - physiology</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Mingyang</creatorcontrib><creatorcontrib>Shan, Haiyan</creatorcontrib><creatorcontrib>Gu, Zhenyong</creatorcontrib><creatorcontrib>Wang, Donglin</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Wang, Zhiwei</creatorcontrib><creatorcontrib>Tao, Luyang</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</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><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Mingyang</au><au>Shan, Haiyan</au><au>Gu, Zhenyong</au><au>Wang, Donglin</au><au>Wang, Tao</au><au>Wang, Zhiwei</au><au>Tao, Luyang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>46</volume><issue>3</issue><spage>631</spage><epage>643</epage><pages>631-643</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Many cellular responses to Ca
2+
signals are mediated by Ca
2+
/calmodulin-dependent enzymes, among which is the Ca
2+
/calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β, γ, and δ. This study aims to investigate changes of CaMKIIδ after traumatic brain injury and its possible role. Rat traumatic brain injury (TBI) model was established by controlled cortical injury system. In the present study, we mainly investigated the expression and cellular localization of CaMKIIδ after traumatic brain injury. Western blot analysis revealed that CaMKIIδ was present in normal rat brain cortex. It gradually increased, reached a peak at the third day after TBI, and then decreased. Importantly, more CaMKIIδ was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3.Importantly, immunohistochemistry analysis revealed that injury-induced expression of CaMKIIδ was colabeled by caspase-3 (apoptosis cells marker). Moreover, pretreatment with the CaMKII inhibitor (KN62) reduced the injury-induced activation of caspase-3. Noticeably, the CaMKII inhibitor KN-62 could reduce TBI-induced cell injury assessed with lesion volume and attenuate behavioral outcome evaluated by motor test. These data suggested that CaMKIIδ may be implicated in the apoptosis of neuron and the recovery of neurological outcomes. However, the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of CaMKIIδ after brain injury.</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>22048920</pmid><doi>10.1007/s12031-011-9651-y</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0895-8696 |
| ispartof | Journal of molecular neuroscience, 2012-03, Vol.46 (3), p.631-643 |
| issn | 0895-8696 1559-1166 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_926884107 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Animals Apoptosis Apoptosis - physiology Biomedical and Life Sciences Biomedicine Brain Injuries - genetics Brain Injuries - metabolism Brain Injuries - pathology Ca super(2+)/calmodulin-dependent protein kinase II Calcium Calcium Signaling - physiology Calcium signalling Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors Calcium-Calmodulin-Dependent Protein Kinase Type 2 - biosynthesis Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics Caspase 3 - metabolism Caspase-3 Cell Biology Cell injury Cortex Data processing Disease Models, Animal Enzyme Inhibitors - pharmacology Enzymes Forensic sciences Gene expression Immunohistochemistry Kinases Laboratory animals Male Nerve Degeneration - metabolism Nerve Degeneration - pathology Nervous system Neurochemistry Neurology Neurons Neurons - metabolism Neurons - pathology Neurosciences Proteins Proteomics Rats Rats, Sprague-Dawley Recovery of Function - physiology Surgery Traumatic brain injury Up-Regulation - physiology Western blotting |
| title | Increased Expression of Calcium/Calmodulin-Dependent Protein Kinase Type II Subunit Delta after Rat Traumatic Brain Injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T18%3A26%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Increased%20Expression%20of%20Calcium/Calmodulin-Dependent%20Protein%20Kinase%20Type%20II%20Subunit%20Delta%20after%20Rat%20Traumatic%20Brain%20Injury&rft.jtitle=Journal%20of%20molecular%20neuroscience&rft.au=Zhang,%20Mingyang&rft.date=2012-03-01&rft.volume=46&rft.issue=3&rft.spage=631&rft.epage=643&rft.pages=631-643&rft.issn=0895-8696&rft.eissn=1559-1166&rft_id=info:doi/10.1007/s12031-011-9651-y&rft_dat=%3Cproquest_cross%3E926884107%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=921577428&rft_id=info:pmid/22048920&rfr_iscdi=true |