Endothelial progenitor cells functionally express inward rectifier potassium channels
Since the first isolation of endothelial progenitor cells (EPCs) from human peripheral blood in 1997, many researchers have conducted studies to understand the characteristics and therapeutic effects of EPCs in vascular disease models. Nevertheless, the electrophysiological properties of EPCs have y...
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description | Since the first isolation of endothelial progenitor cells (EPCs) from human peripheral blood in 1997, many researchers have conducted studies to understand the characteristics and therapeutic effects of EPCs in vascular disease models. Nevertheless, the electrophysiological properties of EPCs have yet to be clearly elucidated. The inward rectifier potassium channel (Kir) performs a major role in controlling the membrane potential and cellular events. Here, via the whole cell patch-clamp technique, we found inwardly rectifying currents in EPCs and that these currents were inhibited by Ba(2+) (100 μM) and Cs(+) (1 mM), known as Kir blockers, in a dose-dependent manner (Ba(2+), 91.2 ± 1.4% at -140 mV and Cs(+), 76.1 ± 6.9% at -140 mV, respectively). Next, using DiBAC(3), a fluorescence indicator of membrane potential, we verified that Ba(2+) induced an increase of fluorescence in EPCs (10 μM, 123 ± 2.8%), implying the depolarization of EPCs. At the mRNA and protein levels, we confirmed the existence of several Kir subtypes, including Kir2.x, 3.x, 4.x, and 6.x. In a functional experiment, we observed that, in the presence of Ba(2+), the number of tubes on Matrigel formed by EPCs was dose-dependently reduced (10 μM, 62.3 ± 6.5%). In addition, the proliferation of EPCs was increased in a dose-dependent fashion (10 μM, 157.9 ± 17.4%), and specific inhibition of Kir2.1 by small interfering RNA also increased the proliferation of EPCs (116.2 ± 2.5%). Our results demonstrate that EPCs express several types of Kir which may modulate the endothelial function and proliferation of EPCs. |
doi_str_mv | 10.1152/ajpcell.00002.2010 |
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Nevertheless, the electrophysiological properties of EPCs have yet to be clearly elucidated. The inward rectifier potassium channel (Kir) performs a major role in controlling the membrane potential and cellular events. Here, via the whole cell patch-clamp technique, we found inwardly rectifying currents in EPCs and that these currents were inhibited by Ba(2+) (100 μM) and Cs(+) (1 mM), known as Kir blockers, in a dose-dependent manner (Ba(2+), 91.2 ± 1.4% at -140 mV and Cs(+), 76.1 ± 6.9% at -140 mV, respectively). Next, using DiBAC(3), a fluorescence indicator of membrane potential, we verified that Ba(2+) induced an increase of fluorescence in EPCs (10 μM, 123 ± 2.8%), implying the depolarization of EPCs. At the mRNA and protein levels, we confirmed the existence of several Kir subtypes, including Kir2.x, 3.x, 4.x, and 6.x. In a functional experiment, we observed that, in the presence of Ba(2+), the number of tubes on Matrigel formed by EPCs was dose-dependently reduced (10 μM, 62.3 ± 6.5%). In addition, the proliferation of EPCs was increased in a dose-dependent fashion (10 μM, 157.9 ± 17.4%), and specific inhibition of Kir2.1 by small interfering RNA also increased the proliferation of EPCs (116.2 ± 2.5%). Our results demonstrate that EPCs express several types of Kir which may modulate the endothelial function and proliferation of EPCs.</description><identifier>ISSN: 0363-6143</identifier><identifier>EISSN: 1522-1563</identifier><identifier>DOI: 10.1152/ajpcell.00002.2010</identifier><identifier>PMID: 21411724</identifier><identifier>CODEN: AJPCDD</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Barium - pharmacology ; Blotting, Western ; Cell Proliferation ; Cells ; Cesium - pharmacology ; Endothelial Cells - metabolism ; Fetal Blood ; Fluorescence ; Fluorescent Antibody Technique ; Humans ; Leukocytes, Mononuclear - metabolism ; Membrane Potentials - drug effects ; Membranes ; Patch-Clamp Techniques ; Phenotype ; Polymerase Chain Reaction ; Potassium ; Potassium - metabolism ; Potassium Channels, Inwardly Rectifying - antagonists & inhibitors ; Potassium Channels, Inwardly Rectifying - genetics ; Potassium Channels, Inwardly Rectifying - metabolism ; Ribonucleic acid ; RNA ; RNA Interference ; RNA, Small Interfering ; Stem Cells - metabolism</subject><ispartof>American Journal of Physiology: Cell Physiology, 2011-07, Vol.301 (1), p.C150-C161</ispartof><rights>Copyright American Physiological Society Jul 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c395t-cc0990d1177b0497dcf29633a0ec5cca79d6de4f5b3d342cd575f626cbcca8553</citedby><cites>FETCH-LOGICAL-c395t-cc0990d1177b0497dcf29633a0ec5cca79d6de4f5b3d342cd575f626cbcca8553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21411724$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jang, Sung-Soo</creatorcontrib><creatorcontrib>Park, Jonghanne</creatorcontrib><creatorcontrib>Hur, Sung Won</creatorcontrib><creatorcontrib>Hong, Yun Hwa</creatorcontrib><creatorcontrib>Hur, Jin</creatorcontrib><creatorcontrib>Chae, Jong Hee</creatorcontrib><creatorcontrib>Kim, Seung Ki</creatorcontrib><creatorcontrib>Kim, Jun</creatorcontrib><creatorcontrib>Kim, Hyo-Soo</creatorcontrib><creatorcontrib>Kim, Sang Jeong</creatorcontrib><title>Endothelial progenitor cells functionally express inward rectifier potassium channels</title><title>American Journal of Physiology: Cell Physiology</title><addtitle>Am J Physiol Cell Physiol</addtitle><description>Since the first isolation of endothelial progenitor cells (EPCs) from human peripheral blood in 1997, many researchers have conducted studies to understand the characteristics and therapeutic effects of EPCs in vascular disease models. Nevertheless, the electrophysiological properties of EPCs have yet to be clearly elucidated. The inward rectifier potassium channel (Kir) performs a major role in controlling the membrane potential and cellular events. Here, via the whole cell patch-clamp technique, we found inwardly rectifying currents in EPCs and that these currents were inhibited by Ba(2+) (100 μM) and Cs(+) (1 mM), known as Kir blockers, in a dose-dependent manner (Ba(2+), 91.2 ± 1.4% at -140 mV and Cs(+), 76.1 ± 6.9% at -140 mV, respectively). Next, using DiBAC(3), a fluorescence indicator of membrane potential, we verified that Ba(2+) induced an increase of fluorescence in EPCs (10 μM, 123 ± 2.8%), implying the depolarization of EPCs. At the mRNA and protein levels, we confirmed the existence of several Kir subtypes, including Kir2.x, 3.x, 4.x, and 6.x. In a functional experiment, we observed that, in the presence of Ba(2+), the number of tubes on Matrigel formed by EPCs was dose-dependently reduced (10 μM, 62.3 ± 6.5%). In addition, the proliferation of EPCs was increased in a dose-dependent fashion (10 μM, 157.9 ± 17.4%), and specific inhibition of Kir2.1 by small interfering RNA also increased the proliferation of EPCs (116.2 ± 2.5%). Our results demonstrate that EPCs express several types of Kir which may modulate the endothelial function and proliferation of EPCs.</description><subject>Barium - pharmacology</subject><subject>Blotting, Western</subject><subject>Cell Proliferation</subject><subject>Cells</subject><subject>Cesium - pharmacology</subject><subject>Endothelial Cells - metabolism</subject><subject>Fetal Blood</subject><subject>Fluorescence</subject><subject>Fluorescent Antibody Technique</subject><subject>Humans</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Membrane Potentials - drug effects</subject><subject>Membranes</subject><subject>Patch-Clamp Techniques</subject><subject>Phenotype</subject><subject>Polymerase Chain Reaction</subject><subject>Potassium</subject><subject>Potassium - metabolism</subject><subject>Potassium Channels, Inwardly Rectifying - antagonists & inhibitors</subject><subject>Potassium Channels, Inwardly Rectifying - genetics</subject><subject>Potassium Channels, Inwardly Rectifying - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Stem Cells - metabolism</subject><issn>0363-6143</issn><issn>1522-1563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkDtPwzAUhS0EoqXwBxhQxMKU4rfrEVXlIVVioXPk2A51lcTBTgT99zi0MHCXO5zvHp17ALhGcI4Qw_dq12lb13OYBs8xRPAETJOAc8Q4OQVTSDjJOaJkAi5i3CWMYi7PwQQjipDAdAo2q9b4fmtrp-qsC_7dtq73IRuNY1YNre6db1Vd7zP71QUbY-baTxVMFmySKmdD1vlexeiGJtNb1ba2jpfgrFJ1tFfHPQObx9Xb8jlfvz69LB_WuSaS9bnWUEpoUhRRQiqF0RWWnBAFrWZaKyENN5ZWrCSGUKwNE6zimOsyiQvGyAzcHXxT8o_Bxr5oXByjq9b6IRYLQdECC4ITefuP3PkhpMdGaMGIkEgmCB8gHXyMwVZFF1yjwr5AsBgrL46VFz-VF2Pl6ejm6DyUjTV_J78dk2-g43_o</recordid><startdate>201107</startdate><enddate>201107</enddate><creator>Jang, Sung-Soo</creator><creator>Park, Jonghanne</creator><creator>Hur, Sung Won</creator><creator>Hong, Yun Hwa</creator><creator>Hur, Jin</creator><creator>Chae, Jong Hee</creator><creator>Kim, Seung Ki</creator><creator>Kim, Jun</creator><creator>Kim, Hyo-Soo</creator><creator>Kim, Sang Jeong</creator><general>American Physiological Society</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>7QP</scope><scope>7TS</scope><scope>7X8</scope></search><sort><creationdate>201107</creationdate><title>Endothelial progenitor cells functionally express inward rectifier potassium channels</title><author>Jang, Sung-Soo ; Park, Jonghanne ; Hur, Sung Won ; Hong, Yun Hwa ; Hur, Jin ; Chae, Jong Hee ; Kim, Seung Ki ; Kim, Jun ; Kim, Hyo-Soo ; Kim, Sang Jeong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c395t-cc0990d1177b0497dcf29633a0ec5cca79d6de4f5b3d342cd575f626cbcca8553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Barium - pharmacology</topic><topic>Blotting, Western</topic><topic>Cell Proliferation</topic><topic>Cells</topic><topic>Cesium - pharmacology</topic><topic>Endothelial Cells - metabolism</topic><topic>Fetal Blood</topic><topic>Fluorescence</topic><topic>Fluorescent Antibody Technique</topic><topic>Humans</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Membrane Potentials - drug effects</topic><topic>Membranes</topic><topic>Patch-Clamp Techniques</topic><topic>Phenotype</topic><topic>Polymerase Chain Reaction</topic><topic>Potassium</topic><topic>Potassium - metabolism</topic><topic>Potassium Channels, Inwardly Rectifying - antagonists & inhibitors</topic><topic>Potassium Channels, Inwardly Rectifying - genetics</topic><topic>Potassium Channels, Inwardly Rectifying - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Stem Cells - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jang, Sung-Soo</creatorcontrib><creatorcontrib>Park, Jonghanne</creatorcontrib><creatorcontrib>Hur, Sung Won</creatorcontrib><creatorcontrib>Hong, Yun Hwa</creatorcontrib><creatorcontrib>Hur, Jin</creatorcontrib><creatorcontrib>Chae, Jong Hee</creatorcontrib><creatorcontrib>Kim, Seung Ki</creatorcontrib><creatorcontrib>Kim, Jun</creatorcontrib><creatorcontrib>Kim, Hyo-Soo</creatorcontrib><creatorcontrib>Kim, Sang Jeong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>MEDLINE - Academic</collection><jtitle>American Journal of Physiology: Cell Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jang, Sung-Soo</au><au>Park, Jonghanne</au><au>Hur, Sung Won</au><au>Hong, Yun Hwa</au><au>Hur, Jin</au><au>Chae, Jong Hee</au><au>Kim, Seung Ki</au><au>Kim, Jun</au><au>Kim, Hyo-Soo</au><au>Kim, Sang Jeong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial progenitor cells functionally express inward rectifier potassium channels</atitle><jtitle>American Journal of Physiology: Cell Physiology</jtitle><addtitle>Am J Physiol Cell Physiol</addtitle><date>2011-07</date><risdate>2011</risdate><volume>301</volume><issue>1</issue><spage>C150</spage><epage>C161</epage><pages>C150-C161</pages><issn>0363-6143</issn><eissn>1522-1563</eissn><coden>AJPCDD</coden><abstract>Since the first isolation of endothelial progenitor cells (EPCs) from human peripheral blood in 1997, many researchers have conducted studies to understand the characteristics and therapeutic effects of EPCs in vascular disease models. Nevertheless, the electrophysiological properties of EPCs have yet to be clearly elucidated. The inward rectifier potassium channel (Kir) performs a major role in controlling the membrane potential and cellular events. Here, via the whole cell patch-clamp technique, we found inwardly rectifying currents in EPCs and that these currents were inhibited by Ba(2+) (100 μM) and Cs(+) (1 mM), known as Kir blockers, in a dose-dependent manner (Ba(2+), 91.2 ± 1.4% at -140 mV and Cs(+), 76.1 ± 6.9% at -140 mV, respectively). Next, using DiBAC(3), a fluorescence indicator of membrane potential, we verified that Ba(2+) induced an increase of fluorescence in EPCs (10 μM, 123 ± 2.8%), implying the depolarization of EPCs. At the mRNA and protein levels, we confirmed the existence of several Kir subtypes, including Kir2.x, 3.x, 4.x, and 6.x. In a functional experiment, we observed that, in the presence of Ba(2+), the number of tubes on Matrigel formed by EPCs was dose-dependently reduced (10 μM, 62.3 ± 6.5%). In addition, the proliferation of EPCs was increased in a dose-dependent fashion (10 μM, 157.9 ± 17.4%), and specific inhibition of Kir2.1 by small interfering RNA also increased the proliferation of EPCs (116.2 ± 2.5%). Our results demonstrate that EPCs express several types of Kir which may modulate the endothelial function and proliferation of EPCs.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>21411724</pmid><doi>10.1152/ajpcell.00002.2010</doi></addata></record> |
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subjects | Barium - pharmacology Blotting, Western Cell Proliferation Cells Cesium - pharmacology Endothelial Cells - metabolism Fetal Blood Fluorescence Fluorescent Antibody Technique Humans Leukocytes, Mononuclear - metabolism Membrane Potentials - drug effects Membranes Patch-Clamp Techniques Phenotype Polymerase Chain Reaction Potassium Potassium - metabolism Potassium Channels, Inwardly Rectifying - antagonists & inhibitors Potassium Channels, Inwardly Rectifying - genetics Potassium Channels, Inwardly Rectifying - metabolism Ribonucleic acid RNA RNA Interference RNA, Small Interfering Stem Cells - metabolism |
title | Endothelial progenitor cells functionally express inward rectifier potassium channels |
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