Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner
Glucocorticoids are hormones released in response to stress that are involved in various physiological processes including immune functions. One immune-modulating mechanism is achieved by the Kv1.3 voltage-dependent potassium channel, which is expressed highly in lymphocytes including effector memor...
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| Veröffentlicht in: | Naunyn-Schmiedeberg's archives of pharmacology 2015-06, Vol.388 (6), p.653-661 |
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| creator | Yu, Jing Park, Mi-Hyeong Choi, Se-Young Jo, Su-Hyun |
| description | Glucocorticoids are hormones released in response to stress that are involved in various physiological processes including immune functions. One immune-modulating mechanism is achieved by the Kv1.3 voltage-dependent potassium channel, which is expressed highly in lymphocytes including effector memory T lymphocytes (T
EM
). Although glucocorticoids are known to inhibit Kv1.3 function, the detailed inhibitory mechanism is not yet fully understood. Here we studied the rapid non-genomic effects of cortisone and hydrocortisone on the human Kv1.3 channel expressed in
Xenopus
oocytes. Both cortisone and hydrocortisone reduced the amplitude of the Kv1.3 channel current in a concentration-dependent manner. Both cortisone and hydrocortisone rapidly and irreversibly inhibited Kv1.3 currents, eliminating the possibility of genomic regulation. Inhibition rate was stable relative to the degree of depolarization. Kinetically, cortisone altered the activating gate of Kv1.3 and hydrocortisone interacted with this channel in an open state. These results suggest that cortisone and hydrocortisone inhibit Kv1.3 currents via a non-genomic mechanism, providing a mechanism for the immunosuppressive effects of glucocorticoids. |
| doi_str_mv | 10.1007/s00210-015-1109-2 |
| format | Article |
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EM
). Although glucocorticoids are known to inhibit Kv1.3 function, the detailed inhibitory mechanism is not yet fully understood. Here we studied the rapid non-genomic effects of cortisone and hydrocortisone on the human Kv1.3 channel expressed in
Xenopus
oocytes. Both cortisone and hydrocortisone reduced the amplitude of the Kv1.3 channel current in a concentration-dependent manner. Both cortisone and hydrocortisone rapidly and irreversibly inhibited Kv1.3 currents, eliminating the possibility of genomic regulation. Inhibition rate was stable relative to the degree of depolarization. Kinetically, cortisone altered the activating gate of Kv1.3 and hydrocortisone interacted with this channel in an open state. These results suggest that cortisone and hydrocortisone inhibit Kv1.3 currents via a non-genomic mechanism, providing a mechanism for the immunosuppressive effects of glucocorticoids.</description><identifier>ISSN: 0028-1298</identifier><identifier>EISSN: 1432-1912</identifier><identifier>DOI: 10.1007/s00210-015-1109-2</identifier><identifier>PMID: 25743574</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cortisone - pharmacology ; Humans ; Hydrocortisone - pharmacology ; Kv1.3 Potassium Channel - genetics ; Kv1.3 Potassium Channel - physiology ; Membrane Potentials - drug effects ; Neurosciences ; Oocytes - drug effects ; Oocytes - physiology ; Original Article ; Pharmacology/Toxicology ; Potassium Channel Blockers - pharmacology ; Xenopus</subject><ispartof>Naunyn-Schmiedeberg's archives of pharmacology, 2015-06, Vol.388 (6), p.653-661</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-2270d3c78da21a71afc249fd652f595a19325c2947f141c9dbf9910b28c5aafb3</citedby><cites>FETCH-LOGICAL-c372t-2270d3c78da21a71afc249fd652f595a19325c2947f141c9dbf9910b28c5aafb3</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/s00210-015-1109-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00210-015-1109-2$$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/25743574$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Jing</creatorcontrib><creatorcontrib>Park, Mi-Hyeong</creatorcontrib><creatorcontrib>Choi, Se-Young</creatorcontrib><creatorcontrib>Jo, Su-Hyun</creatorcontrib><title>Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner</title><title>Naunyn-Schmiedeberg's archives of pharmacology</title><addtitle>Naunyn-Schmiedeberg's Arch Pharmacol</addtitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><description>Glucocorticoids are hormones released in response to stress that are involved in various physiological processes including immune functions. One immune-modulating mechanism is achieved by the Kv1.3 voltage-dependent potassium channel, which is expressed highly in lymphocytes including effector memory T lymphocytes (T
EM
). Although glucocorticoids are known to inhibit Kv1.3 function, the detailed inhibitory mechanism is not yet fully understood. Here we studied the rapid non-genomic effects of cortisone and hydrocortisone on the human Kv1.3 channel expressed in
Xenopus
oocytes. Both cortisone and hydrocortisone reduced the amplitude of the Kv1.3 channel current in a concentration-dependent manner. Both cortisone and hydrocortisone rapidly and irreversibly inhibited Kv1.3 currents, eliminating the possibility of genomic regulation. Inhibition rate was stable relative to the degree of depolarization. Kinetically, cortisone altered the activating gate of Kv1.3 and hydrocortisone interacted with this channel in an open state. These results suggest that cortisone and hydrocortisone inhibit Kv1.3 currents via a non-genomic mechanism, providing a mechanism for the immunosuppressive effects of glucocorticoids.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cortisone - pharmacology</subject><subject>Humans</subject><subject>Hydrocortisone - pharmacology</subject><subject>Kv1.3 Potassium Channel - genetics</subject><subject>Kv1.3 Potassium Channel - physiology</subject><subject>Membrane Potentials - drug effects</subject><subject>Neurosciences</subject><subject>Oocytes - drug effects</subject><subject>Oocytes - physiology</subject><subject>Original Article</subject><subject>Pharmacology/Toxicology</subject><subject>Potassium Channel Blockers - pharmacology</subject><subject>Xenopus</subject><issn>0028-1298</issn><issn>1432-1912</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kE1LxDAURYMoOn78ADdScOMmmvfaTJqlDH6hIIKuQ5qmTmSaaNIOzL83w6iI4CIEcs-7LxxCjoGdA2PiIjGGwCgDTgGYpLhFJlCVSEECbpNJjmsKKOs9sp_SG2NsCpzvkj3koirzmZCnWYiDS8HbQvu2mK_aGMzPk_Nz17ihmI-99sX9Es7LQpvBLd2wymGhCx88fbU-9M4UmfE2HpKdTi-SPfq6D8jL9dXz7JY-PN7czS4fqCkFDhRRsLY0om41ghagO4OV7Nopx45LrkGWyA3KSnRQgZFt00kJrMHacK27pjwgZ5ve9xg-RpsG1btk7GKhvQ1jUjCtsUIBkmX09A_6Fsbo8-_WFNSVFBwyBRvKxJBStJ16j67XcaWAqbVvtfGtsm-19q0wz5x8NY9Nb9ufiW_BGcANkHLkX238tfrf1k90-IlM</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Yu, Jing</creator><creator>Park, Mi-Hyeong</creator><creator>Choi, Se-Young</creator><creator>Jo, Su-Hyun</creator><general>Springer Berlin Heidelberg</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150601</creationdate><title>Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner</title><author>Yu, Jing ; Park, Mi-Hyeong ; Choi, Se-Young ; Jo, Su-Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-2270d3c78da21a71afc249fd652f595a19325c2947f141c9dbf9910b28c5aafb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cortisone - pharmacology</topic><topic>Humans</topic><topic>Hydrocortisone - pharmacology</topic><topic>Kv1.3 Potassium Channel - genetics</topic><topic>Kv1.3 Potassium Channel - physiology</topic><topic>Membrane Potentials - drug effects</topic><topic>Neurosciences</topic><topic>Oocytes - drug effects</topic><topic>Oocytes - physiology</topic><topic>Original Article</topic><topic>Pharmacology/Toxicology</topic><topic>Potassium Channel Blockers - pharmacology</topic><topic>Xenopus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Jing</creatorcontrib><creatorcontrib>Park, Mi-Hyeong</creatorcontrib><creatorcontrib>Choi, Se-Young</creatorcontrib><creatorcontrib>Jo, Su-Hyun</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Jing</au><au>Park, Mi-Hyeong</au><au>Choi, Se-Young</au><au>Jo, Su-Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner</atitle><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle><stitle>Naunyn-Schmiedeberg's Arch Pharmacol</stitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>388</volume><issue>6</issue><spage>653</spage><epage>661</epage><pages>653-661</pages><issn>0028-1298</issn><eissn>1432-1912</eissn><abstract>Glucocorticoids are hormones released in response to stress that are involved in various physiological processes including immune functions. One immune-modulating mechanism is achieved by the Kv1.3 voltage-dependent potassium channel, which is expressed highly in lymphocytes including effector memory T lymphocytes (T
EM
). Although glucocorticoids are known to inhibit Kv1.3 function, the detailed inhibitory mechanism is not yet fully understood. Here we studied the rapid non-genomic effects of cortisone and hydrocortisone on the human Kv1.3 channel expressed in
Xenopus
oocytes. Both cortisone and hydrocortisone reduced the amplitude of the Kv1.3 channel current in a concentration-dependent manner. Both cortisone and hydrocortisone rapidly and irreversibly inhibited Kv1.3 currents, eliminating the possibility of genomic regulation. Inhibition rate was stable relative to the degree of depolarization. Kinetically, cortisone altered the activating gate of Kv1.3 and hydrocortisone interacted with this channel in an open state. These results suggest that cortisone and hydrocortisone inhibit Kv1.3 currents via a non-genomic mechanism, providing a mechanism for the immunosuppressive effects of glucocorticoids.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25743574</pmid><doi>10.1007/s00210-015-1109-2</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Cortisone - pharmacology Humans Hydrocortisone - pharmacology Kv1.3 Potassium Channel - genetics Kv1.3 Potassium Channel - physiology Membrane Potentials - drug effects Neurosciences Oocytes - drug effects Oocytes - physiology Original Article Pharmacology/Toxicology Potassium Channel Blockers - pharmacology Xenopus |
| title | Cortisone and hydrocortisone inhibit human Kv1.3 activity in a non-genomic manner |
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