P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose

P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose

Hyperglycemia is associated with increased risk of cardiovascular disease. Recent studies have suggested that the daily intake of large amounts of marine oils rich in omega-3 polyunsaturated fatty acids (including EPA) decreases the incidence of cardiovascular disease and coronary artery disease. Ho...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:American journal of hypertension 2002-04, Vol.15 (S3), p.101A-101A
Hauptverfasser: Yamamoto, Kei, Smutko, Victoria, Matsumoto, Keiko, Nyby, Michael D., Tuck, Michael L.
Format: Artikel
Sprache:eng
Schlagworte:
Apoptosis
Cell death
Diabetes
Eicosapentaeoic Acid
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 101A
container_issue S3
container_start_page 101A
container_title American journal of hypertension
container_volume 15
creator Yamamoto, Kei
Smutko, Victoria
Matsumoto, Keiko
Nyby, Michael D.
Tuck, Michael L.
description Hyperglycemia is associated with increased risk of cardiovascular disease. Recent studies have suggested that the daily intake of large amounts of marine oils rich in omega-3 polyunsaturated fatty acids (including EPA) decreases the incidence of cardiovascular disease and coronary artery disease. However, the mechanism by which EPA exerts this cardioprotective effect has not been determined. The purpose of this study was to investigate the cellular mechanism by which EPA protects human coronary artery endothelial cells (HCAEC) from hyperglycemia-induced cell death. HCAEC (provided by Cell Systems, Kirkland, WA) were cultured in CSC medium. Cell number was estimated by assessing the rate of [3H]-Thymidine uptake. Cell death was assessed by lactate dehydrogenase (LDH) enzyme activity and caspase-3 activity assays. When HCAEC were exposed to high glucose (33mM) for 96 hr, the number of HCAEC as measured by [3H]-Thymidine uptake was decreased to 75.6±7.4% (P
doi_str_mv 10.1016/S0895-7061(02)02553-0
format Article
fullrecord <record><control><sourceid>proquest_natur</sourceid><recordid>TN_cdi_proquest_journals_1026591961</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2712854331</sourcerecordid><originalsourceid>FETCH-LOGICAL-i911-843763b3b461104365003dae959ef43e9ba647519cd35fc52418b07f97159c0b3</originalsourceid><addsrcrecordid>eNpFzUtLw0AUBeBBFKzVnyAMuGkX0XvnlY67UqsVKhbsorgJk8mkmRqTmEex_95ARVdncT7OIeQa4RYB1d0bTLQMQlA4AjYGJiUP4IQMUAsMQsbkKRn8kXNy0TQ7ABBK4YDYVcCA3dO5t2VjKle0xhWlt9RYn9DRfDUd06p2-75o6N40tstNTV2RlG3mcm9yal2e08SZNqO-SDrrEhofaOa3Gd3mXb_qLslZavLGXf3mkKwf5-vZIli-Pj3PpsvAa8RgInioeMxjoRBBcCUBeGKcltqlgjsdGyVCidomXKZWMoGTGMJUhyi1hZgPyc1xtqrLr841bbQru7roHyMEpqRGrbBX9KgK03a1i6raf5r6EJldxgCY0KwnwZH4pnXf_6L-iFTIQxktNu_Rw8uGLZneRJL_AOdwb8g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1026591961</pqid></control><display><type>article</type><title>P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Yamamoto, Kei ; Smutko, Victoria ; Matsumoto, Keiko ; Nyby, Michael D. ; Tuck, Michael L.</creator><creatorcontrib>Yamamoto, Kei ; Smutko, Victoria ; Matsumoto, Keiko ; Nyby, Michael D. ; Tuck, Michael L.</creatorcontrib><description>Hyperglycemia is associated with increased risk of cardiovascular disease. Recent studies have suggested that the daily intake of large amounts of marine oils rich in omega-3 polyunsaturated fatty acids (including EPA) decreases the incidence of cardiovascular disease and coronary artery disease. However, the mechanism by which EPA exerts this cardioprotective effect has not been determined. The purpose of this study was to investigate the cellular mechanism by which EPA protects human coronary artery endothelial cells (HCAEC) from hyperglycemia-induced cell death. HCAEC (provided by Cell Systems, Kirkland, WA) were cultured in CSC medium. Cell number was estimated by assessing the rate of [3H]-Thymidine uptake. Cell death was assessed by lactate dehydrogenase (LDH) enzyme activity and caspase-3 activity assays. When HCAEC were exposed to high glucose (33mM) for 96 hr, the number of HCAEC as measured by [3H]-Thymidine uptake was decreased to 75.6±7.4% (P&lt;0.05) of the number exposed to normal glucose (5 mM). Addition of EPA (1–10 μM) during the high-glucose exposure, prevented this decrease of cell number in a dose-dependent manner (1 μM EPA, 85.4±9.0% of control; 5 μM EPA, 95.3±10.4%, P&lt;0.05 from high glucose without EPA). In additon, 33 mM mannitol did not change cell number from that observed with normal glucose (5mM). LDH and caspase activity assays confirmed that high glucose caused HCAEC cell death (apoptosis and necrosis combined). LDH released to the media by HCAEC was increased by high glucose to 161±3.3% of that released in normal glucose (P&lt;0.05). EPA prevented this high glucose-induced LDH release in a dose-dependent manner (1 μM EPA, 130±3.3% of normal; 5μM EPA, 101±10.1% of control, P&lt;0.05 from high glucose with no EPA). Also, EPA prevented the increase of caspase activity induced by high glucose. Exposure of HCAEC to high glucose (33 mM) caused caspase-3 activity to increase 14-fold above that of HCAEC exposed to normal glucose. EPA (5 μM) inhibited this increase of caspase-3 activity to 2.6-fold (P&lt;0.05 compared to high glucose with no EPA). These results demonstrate that high glucose concentrations can stimulate cell death of HCAEC in culture and that this cell death can be prevented by EPA. Our results suggest that EPA improves cardiovascular health, especially in patients with hyperglycemia, by inhibiting the pathway which results in the activation of caspase-3.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1941-7225</identifier><identifier>EISSN: 1879-1905</identifier><identifier>DOI: 10.1016/S0895-7061(02)02553-0</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Apoptosis ; Cell death ; Diabetes ; Eicosapentaeoic Acid</subject><ispartof>American journal of hypertension, 2002-04, Vol.15 (S3), p.101A-101A</ispartof><rights>Copyright Nature Publishing Group Apr 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Yamamoto, Kei</creatorcontrib><creatorcontrib>Smutko, Victoria</creatorcontrib><creatorcontrib>Matsumoto, Keiko</creatorcontrib><creatorcontrib>Nyby, Michael D.</creatorcontrib><creatorcontrib>Tuck, Michael L.</creatorcontrib><title>P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>Hyperglycemia is associated with increased risk of cardiovascular disease. Recent studies have suggested that the daily intake of large amounts of marine oils rich in omega-3 polyunsaturated fatty acids (including EPA) decreases the incidence of cardiovascular disease and coronary artery disease. However, the mechanism by which EPA exerts this cardioprotective effect has not been determined. The purpose of this study was to investigate the cellular mechanism by which EPA protects human coronary artery endothelial cells (HCAEC) from hyperglycemia-induced cell death. HCAEC (provided by Cell Systems, Kirkland, WA) were cultured in CSC medium. Cell number was estimated by assessing the rate of [3H]-Thymidine uptake. Cell death was assessed by lactate dehydrogenase (LDH) enzyme activity and caspase-3 activity assays. When HCAEC were exposed to high glucose (33mM) for 96 hr, the number of HCAEC as measured by [3H]-Thymidine uptake was decreased to 75.6±7.4% (P&lt;0.05) of the number exposed to normal glucose (5 mM). Addition of EPA (1–10 μM) during the high-glucose exposure, prevented this decrease of cell number in a dose-dependent manner (1 μM EPA, 85.4±9.0% of control; 5 μM EPA, 95.3±10.4%, P&lt;0.05 from high glucose without EPA). In additon, 33 mM mannitol did not change cell number from that observed with normal glucose (5mM). LDH and caspase activity assays confirmed that high glucose caused HCAEC cell death (apoptosis and necrosis combined). LDH released to the media by HCAEC was increased by high glucose to 161±3.3% of that released in normal glucose (P&lt;0.05). EPA prevented this high glucose-induced LDH release in a dose-dependent manner (1 μM EPA, 130±3.3% of normal; 5μM EPA, 101±10.1% of control, P&lt;0.05 from high glucose with no EPA). Also, EPA prevented the increase of caspase activity induced by high glucose. Exposure of HCAEC to high glucose (33 mM) caused caspase-3 activity to increase 14-fold above that of HCAEC exposed to normal glucose. EPA (5 μM) inhibited this increase of caspase-3 activity to 2.6-fold (P&lt;0.05 compared to high glucose with no EPA). These results demonstrate that high glucose concentrations can stimulate cell death of HCAEC in culture and that this cell death can be prevented by EPA. Our results suggest that EPA improves cardiovascular health, especially in patients with hyperglycemia, by inhibiting the pathway which results in the activation of caspase-3.</description><subject>Apoptosis</subject><subject>Cell death</subject><subject>Diabetes</subject><subject>Eicosapentaeoic Acid</subject><issn>0895-7061</issn><issn>1941-7225</issn><issn>1879-1905</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpFzUtLw0AUBeBBFKzVnyAMuGkX0XvnlY67UqsVKhbsorgJk8mkmRqTmEex_95ARVdncT7OIeQa4RYB1d0bTLQMQlA4AjYGJiUP4IQMUAsMQsbkKRn8kXNy0TQ7ABBK4YDYVcCA3dO5t2VjKle0xhWlt9RYn9DRfDUd06p2-75o6N40tstNTV2RlG3mcm9yal2e08SZNqO-SDrrEhofaOa3Gd3mXb_qLslZavLGXf3mkKwf5-vZIli-Pj3PpsvAa8RgInioeMxjoRBBcCUBeGKcltqlgjsdGyVCidomXKZWMoGTGMJUhyi1hZgPyc1xtqrLr841bbQru7roHyMEpqRGrbBX9KgK03a1i6raf5r6EJldxgCY0KwnwZH4pnXf_6L-iFTIQxktNu_Rw8uGLZneRJL_AOdwb8g</recordid><startdate>200204</startdate><enddate>200204</enddate><creator>Yamamoto, Kei</creator><creator>Smutko, Victoria</creator><creator>Matsumoto, Keiko</creator><creator>Nyby, Michael D.</creator><creator>Tuck, Michael L.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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></search><sort><creationdate>200204</creationdate><title>P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose</title><author>Yamamoto, Kei ; Smutko, Victoria ; Matsumoto, Keiko ; Nyby, Michael D. ; Tuck, Michael L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i911-843763b3b461104365003dae959ef43e9ba647519cd35fc52418b07f97159c0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Apoptosis</topic><topic>Cell death</topic><topic>Diabetes</topic><topic>Eicosapentaeoic Acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamamoto, Kei</creatorcontrib><creatorcontrib>Smutko, Victoria</creatorcontrib><creatorcontrib>Matsumoto, Keiko</creatorcontrib><creatorcontrib>Nyby, Michael D.</creatorcontrib><creatorcontrib>Tuck, Michael L.</creatorcontrib><collection>Istex</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 &amp; Medical Complete (Alumni)</collection><collection>Health &amp; 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><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamamoto, Kei</au><au>Smutko, Victoria</au><au>Matsumoto, Keiko</au><au>Nyby, Michael D.</au><au>Tuck, Michael L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2002-04</date><risdate>2002</risdate><volume>15</volume><issue>S3</issue><spage>101A</spage><epage>101A</epage><pages>101A-101A</pages><issn>0895-7061</issn><eissn>1941-7225</eissn><eissn>1879-1905</eissn><coden>AJHYE6</coden><abstract>Hyperglycemia is associated with increased risk of cardiovascular disease. Recent studies have suggested that the daily intake of large amounts of marine oils rich in omega-3 polyunsaturated fatty acids (including EPA) decreases the incidence of cardiovascular disease and coronary artery disease. However, the mechanism by which EPA exerts this cardioprotective effect has not been determined. The purpose of this study was to investigate the cellular mechanism by which EPA protects human coronary artery endothelial cells (HCAEC) from hyperglycemia-induced cell death. HCAEC (provided by Cell Systems, Kirkland, WA) were cultured in CSC medium. Cell number was estimated by assessing the rate of [3H]-Thymidine uptake. Cell death was assessed by lactate dehydrogenase (LDH) enzyme activity and caspase-3 activity assays. When HCAEC were exposed to high glucose (33mM) for 96 hr, the number of HCAEC as measured by [3H]-Thymidine uptake was decreased to 75.6±7.4% (P&lt;0.05) of the number exposed to normal glucose (5 mM). Addition of EPA (1–10 μM) during the high-glucose exposure, prevented this decrease of cell number in a dose-dependent manner (1 μM EPA, 85.4±9.0% of control; 5 μM EPA, 95.3±10.4%, P&lt;0.05 from high glucose without EPA). In additon, 33 mM mannitol did not change cell number from that observed with normal glucose (5mM). LDH and caspase activity assays confirmed that high glucose caused HCAEC cell death (apoptosis and necrosis combined). LDH released to the media by HCAEC was increased by high glucose to 161±3.3% of that released in normal glucose (P&lt;0.05). EPA prevented this high glucose-induced LDH release in a dose-dependent manner (1 μM EPA, 130±3.3% of normal; 5μM EPA, 101±10.1% of control, P&lt;0.05 from high glucose with no EPA). Also, EPA prevented the increase of caspase activity induced by high glucose. Exposure of HCAEC to high glucose (33 mM) caused caspase-3 activity to increase 14-fold above that of HCAEC exposed to normal glucose. EPA (5 μM) inhibited this increase of caspase-3 activity to 2.6-fold (P&lt;0.05 compared to high glucose with no EPA). These results demonstrate that high glucose concentrations can stimulate cell death of HCAEC in culture and that this cell death can be prevented by EPA. Our results suggest that EPA improves cardiovascular health, especially in patients with hyperglycemia, by inhibiting the pathway which results in the activation of caspase-3.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><doi>10.1016/S0895-7061(02)02553-0</doi></addata></record>
fulltext fulltext
identifier ISSN: 0895-7061
ispartof American journal of hypertension, 2002-04, Vol.15 (S3), p.101A-101A
issn 0895-7061
1941-7225
1879-1905
language eng
recordid cdi_proquest_journals_1026591961
source Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection
subjects Apoptosis
Cell death
Diabetes
Eicosapentaeoic Acid
title P-202: Eicosapentaenoic acid (EPA) prevents vascular endothelial cell death induced by high glucose
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T11%3A18%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_natur&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=P-202:%20Eicosapentaenoic%20acid%20(EPA)%20prevents%20vascular%20endothelial%20cell%20death%20induced%20by%20high%20glucose&rft.jtitle=American%20journal%20of%20hypertension&rft.au=Yamamoto,%20Kei&rft.date=2002-04&rft.volume=15&rft.issue=S3&rft.spage=101A&rft.epage=101A&rft.pages=101A-101A&rft.issn=0895-7061&rft.eissn=1941-7225&rft.coden=AJHYE6&rft_id=info:doi/10.1016/S0895-7061(02)02553-0&rft_dat=%3Cproquest_natur%3E2712854331%3C/proquest_natur%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1026591961&rft_id=info:pmid/&rfr_iscdi=true