TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons
The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that con...
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| Veröffentlicht in: | Molecular medicine reports 2012-04, Vol.5 (4), p.1049-1052 |
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| creator | ZHOU, JUN YAO, SHANG-LONG YANG, CHENG-XIANG ZHONG, JI-YING WANG, HAN-BING ZHANG, YAN |
| description | The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin-mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP. |
| doi_str_mv | 10.3892/mmr.2012.778 |
| format | Article |
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TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin-mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2012.778</identifier><identifier>PMID: 22307830</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adenoviridae - genetics ; Adenoviruses ; Animals ; Antibodies ; Antipruritics - pharmacology ; Biotechnology ; Capsaicin ; Capsaicin - pharmacology ; Cells, Cultured ; Dorsal root ganglia ; dorsal root ganglion neuron ; Ganglia, Spinal - cytology ; Ganglia, Spinal - drug effects ; Genetic Vectors ; Membrane potential ; mRNA ; Nervous system ; Neurons ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Peripheral neuropathy ; Potassium ; Potassium channels ; Potassium Channels - genetics ; Potassium Channels - metabolism ; Proteins ; Radioimmunoassay ; Rats ; Rats, Sprague-Dawley ; Substance P ; Substance P - metabolism ; subtance P release ; TRESK</subject><ispartof>Molecular medicine reports, 2012-04, Vol.5 (4), p.1049-1052</ispartof><rights>Copyright © 2012, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2012</rights><rights>Copyright © 2012, Spandidos Publications 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-92c1dcf295a024cf159b167c55983657617b7a2f80838e5c099f14a980556ca3</citedby><cites>FETCH-LOGICAL-c443t-92c1dcf295a024cf159b167c55983657617b7a2f80838e5c099f14a980556ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22307830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHOU, JUN</creatorcontrib><creatorcontrib>YAO, SHANG-LONG</creatorcontrib><creatorcontrib>YANG, CHENG-XIANG</creatorcontrib><creatorcontrib>ZHONG, JI-YING</creatorcontrib><creatorcontrib>WANG, HAN-BING</creatorcontrib><creatorcontrib>ZHANG, YAN</creatorcontrib><title>TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin-mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP.</description><subject>Adenoviridae - genetics</subject><subject>Adenoviruses</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antipruritics - pharmacology</subject><subject>Biotechnology</subject><subject>Capsaicin</subject><subject>Capsaicin - pharmacology</subject><subject>Cells, Cultured</subject><subject>Dorsal root ganglia</subject><subject>dorsal root ganglion neuron</subject><subject>Ganglia, Spinal - cytology</subject><subject>Ganglia, Spinal - drug effects</subject><subject>Genetic Vectors</subject><subject>Membrane potential</subject><subject>mRNA</subject><subject>Nervous system</subject><subject>Neurons</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Peripheral neuropathy</subject><subject>Potassium</subject><subject>Potassium channels</subject><subject>Potassium Channels - genetics</subject><subject>Potassium Channels - metabolism</subject><subject>Proteins</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Substance P</subject><subject>Substance P - metabolism</subject><subject>subtance P release</subject><subject>TRESK</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkU1rFDEch4Motl29eZaABy_OmpfJJLkIpdQqFhTde_hPJrNNmUnWJLPgJ_Brm6Xr-nJKIA8Pv_Ag9IKSNVeavZ3ntGaEsrWU6hE6p1LThhPSPj7emdbyDF3kfE9IJ5jQT9EZY5xIxck5-rn5ev3tE9664HByNs69DxAKhsGFuPdpyXjvbIkJ-3Dne18ytrDL4K0PzewGD8UNOC99LhCsw1-qZXKQHR5TnLFdprKkSiQoeIgpw4RTjAVvIWwnHwMObkkx5GfoyQhTds-P5wpt3l9vrj40t59vPl5d3ja2bXlpNLN0sCPTAghr7UiF7mknrRBa8U7IjspeAhsVUVw5YYnWI21BKyJEZ4Gv0LsH7W7p63rrQkkwmV3yM6QfJoI3_74Ef2e2cW94qznhrApeHwUpfl9cLmb22bppguDiko1mtGXqQK_Qq__I-7ikUD9nmOwEbxWp4Aq9eaBsijknN562UGIOfU3taw59Te1b8Zd_7z_Bv4P-2Zd3EAY_xHxiqqghoiFtQ0nd9wsSKLC5</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>ZHOU, JUN</creator><creator>YAO, SHANG-LONG</creator><creator>YANG, CHENG-XIANG</creator><creator>ZHONG, JI-YING</creator><creator>WANG, HAN-BING</creator><creator>ZHANG, YAN</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK 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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120401</creationdate><title>TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons</title><author>ZHOU, JUN ; YAO, SHANG-LONG ; YANG, CHENG-XIANG ; ZHONG, JI-YING ; WANG, HAN-BING ; ZHANG, YAN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-92c1dcf295a024cf159b167c55983657617b7a2f80838e5c099f14a980556ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenoviridae - genetics</topic><topic>Adenoviruses</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antipruritics - pharmacology</topic><topic>Biotechnology</topic><topic>Capsaicin</topic><topic>Capsaicin - pharmacology</topic><topic>Cells, Cultured</topic><topic>Dorsal root ganglia</topic><topic>dorsal root ganglion neuron</topic><topic>Ganglia, Spinal - cytology</topic><topic>Ganglia, Spinal - drug effects</topic><topic>Genetic Vectors</topic><topic>Membrane potential</topic><topic>mRNA</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Peripheral neuropathy</topic><topic>Potassium</topic><topic>Potassium channels</topic><topic>Potassium Channels - genetics</topic><topic>Potassium Channels - metabolism</topic><topic>Proteins</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Substance P</topic><topic>Substance P - metabolism</topic><topic>subtance P release</topic><topic>TRESK</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHOU, JUN</creatorcontrib><creatorcontrib>YAO, SHANG-LONG</creatorcontrib><creatorcontrib>YANG, CHENG-XIANG</creatorcontrib><creatorcontrib>ZHONG, JI-YING</creatorcontrib><creatorcontrib>WANG, HAN-BING</creatorcontrib><creatorcontrib>ZHANG, YAN</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>British Nursing Database</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>Biological Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHOU, JUN</au><au>YAO, SHANG-LONG</au><au>YANG, CHENG-XIANG</au><au>ZHONG, JI-YING</au><au>WANG, HAN-BING</au><au>ZHANG, YAN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>5</volume><issue>4</issue><spage>1049</spage><epage>1052</epage><pages>1049-1052</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin-mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>22307830</pmid><doi>10.3892/mmr.2012.778</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2012-04, Vol.5 (4), p.1049-1052 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adenoviridae - genetics Adenoviruses Animals Antibodies Antipruritics - pharmacology Biotechnology Capsaicin Capsaicin - pharmacology Cells, Cultured Dorsal root ganglia dorsal root ganglion neuron Ganglia, Spinal - cytology Ganglia, Spinal - drug effects Genetic Vectors Membrane potential mRNA Nervous system Neurons Neurons - cytology Neurons - drug effects Neurons - metabolism Peripheral neuropathy Potassium Potassium channels Potassium Channels - genetics Potassium Channels - metabolism Proteins Radioimmunoassay Rats Rats, Sprague-Dawley Substance P Substance P - metabolism subtance P release TRESK |
| title | TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons |
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