Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells
During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury,...
Gespeichert in:
| Veröffentlicht in: | Journal of molecular and cellular cardiology 1998-12, Vol.30 (12), p.2739-2749 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2749 |
|---|---|
| container_issue | 12 |
| container_start_page | 2739 |
| container_title | Journal of molecular and cellular cardiology |
| container_volume | 30 |
| creator | Gill, Richard R. Gbur, Jr, Charles J. Fisher, Bernard J. Hess, Michael L. Fowler, III, Alpha A. Kukreja, Rakesh C. Sholley, Milton M. |
| description | During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury, possibly via increased synthesis of heat shock proteins (HSPs). We hypothesized that heat shock preconditioning may protect human endothelial cells against oxidative damage. Cultured human umbilical vein endothelial cells (HUVEC) were subjected to heat shock (42°C, 1 h) and allowed to recover for 2 or 20 h, at which times the cells were oxidatively stressed for 1 h by exposing them to 100–200μmol/l of hydrogen peroxide (H2O2). Cellular damage was assessed immediately and 18 h later by morphology and release of lactate dehydrogenase (LDH). No protection of HUVEC was seen using the 2-hour recovery interval, but a significant protection (P |
| doi_str_mv | 10.1006/jmcc.1998.0837 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69176925</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0022282898908379</els_id><sourcerecordid>69176925</sourcerecordid><originalsourceid>FETCH-LOGICAL-c339t-a9882509bcb85939c9ebdf35bf41c6f28b49599566cd0032c42d38e4b2b3c7ed3</originalsourceid><addsrcrecordid>eNp1kM1vEzEQxa0KVELhyg3JJ24bvPZ64zmiUJpKlYoE5Wr5Y7Z12I9ieyPy39erRNw4jfTem6eZHyEfarauGWs_7wfn1jWAWjMlNhdkVTOQlZKqeUVWjHFeccXVG_I2pT1jDBohLsklADDZNCsSd2gy_fE0ud_0e5wOwWOiX7E3R_SLkNHlMI3UPJowpkzv_wZvcjggvR33czzSMNLt3Oc5lvxuHsxIHwYb-uBMT39hca9HP-Un7EMRttj36R153Zk-4fvzvCIP365_bnfV3f3N7fbLXeWEgFwZUIpLBtZZJUGAA7S-E9J2Te3ajivbgASQbes8Y4K7hnuhsLHcCrdBL67Ip1Pvc5z-zJiyHkJy5QIz4jQn3UK9aYHLElyfgi5OKUXs9HMMg4lHXTO9QNYLZL1A1gvksvDx3DzbAf2_-Jlq8dXJx_LeIWDUyQUcHfoQC0_tp_C_6hdbwYzA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69176925</pqid></control><display><type>article</type><title>Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Gill, Richard R. ; Gbur, Jr, Charles J. ; Fisher, Bernard J. ; Hess, Michael L. ; Fowler, III, Alpha A. ; Kukreja, Rakesh C. ; Sholley, Milton M.</creator><creatorcontrib>Gill, Richard R. ; Gbur, Jr, Charles J. ; Fisher, Bernard J. ; Hess, Michael L. ; Fowler, III, Alpha A. ; Kukreja, Rakesh C. ; Sholley, Milton M.</creatorcontrib><description>During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury, possibly via increased synthesis of heat shock proteins (HSPs). We hypothesized that heat shock preconditioning may protect human endothelial cells against oxidative damage. Cultured human umbilical vein endothelial cells (HUVEC) were subjected to heat shock (42°C, 1 h) and allowed to recover for 2 or 20 h, at which times the cells were oxidatively stressed for 1 h by exposing them to 100–200μmol/l of hydrogen peroxide (H2O2). Cellular damage was assessed immediately and 18 h later by morphology and release of lactate dehydrogenase (LDH). No protection of HUVEC was seen using the 2-hour recovery interval, but a significant protection (P<0.05) was observed after the 20-hour delay. Northern blot analysis at 1 and 2 h after heating showed induction of HSP-70 mRNA. Western blot analysis demonstrated a significant increase in HSP-72 protein after 2 as well as 20 h of recovery from heat shock, although the amounts of protein at the two times were not significantly different. Furthermore, no differences in the activity of the antioxidant enzyme catalase were observed between heated and unheated HUVEC at 2 and 20 h after heat preconditioning. Thus, heat shock preconditioning inducesdelayedprotection against oxidative injury in HUVEC, and the mechanism of protection appears to involve more than the expression of HSP-72 or activity of catalase.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.1998.0837</identifier><identifier>PMID: 9990544</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Blotting, Northern ; Blotting, Western ; Catalase - physiology ; Cell culture ; Cells, Cultured ; Dose-Response Relationship, Drug ; Endothelial cells ; Endothelium, Vascular - physiology ; Heat shock proteins ; Heat-Shock Proteins - pharmacology ; Heat-Shock Response - physiology ; HSP72 Heat-Shock Proteins ; Humans ; Hydrogen Peroxide - pharmacology ; L-Lactate Dehydrogenase - analysis ; Oxidative injury ; Oxidative Stress - physiology ; Preconditioning ; Temperature ; Time Factors ; Umbilical Veins - physiology</subject><ispartof>Journal of molecular and cellular cardiology, 1998-12, Vol.30 (12), p.2739-2749</ispartof><rights>1998 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c339t-a9882509bcb85939c9ebdf35bf41c6f28b49599566cd0032c42d38e4b2b3c7ed3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282898908379$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9990544$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gill, Richard R.</creatorcontrib><creatorcontrib>Gbur, Jr, Charles J.</creatorcontrib><creatorcontrib>Fisher, Bernard J.</creatorcontrib><creatorcontrib>Hess, Michael L.</creatorcontrib><creatorcontrib>Fowler, III, Alpha A.</creatorcontrib><creatorcontrib>Kukreja, Rakesh C.</creatorcontrib><creatorcontrib>Sholley, Milton M.</creatorcontrib><title>Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury, possibly via increased synthesis of heat shock proteins (HSPs). We hypothesized that heat shock preconditioning may protect human endothelial cells against oxidative damage. Cultured human umbilical vein endothelial cells (HUVEC) were subjected to heat shock (42°C, 1 h) and allowed to recover for 2 or 20 h, at which times the cells were oxidatively stressed for 1 h by exposing them to 100–200μmol/l of hydrogen peroxide (H2O2). Cellular damage was assessed immediately and 18 h later by morphology and release of lactate dehydrogenase (LDH). No protection of HUVEC was seen using the 2-hour recovery interval, but a significant protection (P<0.05) was observed after the 20-hour delay. Northern blot analysis at 1 and 2 h after heating showed induction of HSP-70 mRNA. Western blot analysis demonstrated a significant increase in HSP-72 protein after 2 as well as 20 h of recovery from heat shock, although the amounts of protein at the two times were not significantly different. Furthermore, no differences in the activity of the antioxidant enzyme catalase were observed between heated and unheated HUVEC at 2 and 20 h after heat preconditioning. Thus, heat shock preconditioning inducesdelayedprotection against oxidative injury in HUVEC, and the mechanism of protection appears to involve more than the expression of HSP-72 or activity of catalase.</description><subject>Blotting, Northern</subject><subject>Blotting, Western</subject><subject>Catalase - physiology</subject><subject>Cell culture</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial cells</subject><subject>Endothelium, Vascular - physiology</subject><subject>Heat shock proteins</subject><subject>Heat-Shock Proteins - pharmacology</subject><subject>Heat-Shock Response - physiology</subject><subject>HSP72 Heat-Shock Proteins</subject><subject>Humans</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>L-Lactate Dehydrogenase - analysis</subject><subject>Oxidative injury</subject><subject>Oxidative Stress - physiology</subject><subject>Preconditioning</subject><subject>Temperature</subject><subject>Time Factors</subject><subject>Umbilical Veins - physiology</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1vEzEQxa0KVELhyg3JJ24bvPZ64zmiUJpKlYoE5Wr5Y7Z12I9ieyPy39erRNw4jfTem6eZHyEfarauGWs_7wfn1jWAWjMlNhdkVTOQlZKqeUVWjHFeccXVG_I2pT1jDBohLsklADDZNCsSd2gy_fE0ud_0e5wOwWOiX7E3R_SLkNHlMI3UPJowpkzv_wZvcjggvR33czzSMNLt3Oc5lvxuHsxIHwYb-uBMT39hca9HP-Un7EMRttj36R153Zk-4fvzvCIP365_bnfV3f3N7fbLXeWEgFwZUIpLBtZZJUGAA7S-E9J2Te3ajivbgASQbes8Y4K7hnuhsLHcCrdBL67Ip1Pvc5z-zJiyHkJy5QIz4jQn3UK9aYHLElyfgi5OKUXs9HMMg4lHXTO9QNYLZL1A1gvksvDx3DzbAf2_-Jlq8dXJx_LeIWDUyQUcHfoQC0_tp_C_6hdbwYzA</recordid><startdate>19981201</startdate><enddate>19981201</enddate><creator>Gill, Richard R.</creator><creator>Gbur, Jr, Charles J.</creator><creator>Fisher, Bernard J.</creator><creator>Hess, Michael L.</creator><creator>Fowler, III, Alpha A.</creator><creator>Kukreja, Rakesh C.</creator><creator>Sholley, Milton M.</creator><general>Elsevier 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>7X8</scope></search><sort><creationdate>19981201</creationdate><title>Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells</title><author>Gill, Richard R. ; Gbur, Jr, Charles J. ; Fisher, Bernard J. ; Hess, Michael L. ; Fowler, III, Alpha A. ; Kukreja, Rakesh C. ; Sholley, Milton M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-a9882509bcb85939c9ebdf35bf41c6f28b49599566cd0032c42d38e4b2b3c7ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Blotting, Northern</topic><topic>Blotting, Western</topic><topic>Catalase - physiology</topic><topic>Cell culture</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelial cells</topic><topic>Endothelium, Vascular - physiology</topic><topic>Heat shock proteins</topic><topic>Heat-Shock Proteins - pharmacology</topic><topic>Heat-Shock Response - physiology</topic><topic>HSP72 Heat-Shock Proteins</topic><topic>Humans</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>L-Lactate Dehydrogenase - analysis</topic><topic>Oxidative injury</topic><topic>Oxidative Stress - physiology</topic><topic>Preconditioning</topic><topic>Temperature</topic><topic>Time Factors</topic><topic>Umbilical Veins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gill, Richard R.</creatorcontrib><creatorcontrib>Gbur, Jr, Charles J.</creatorcontrib><creatorcontrib>Fisher, Bernard J.</creatorcontrib><creatorcontrib>Hess, Michael L.</creatorcontrib><creatorcontrib>Fowler, III, Alpha A.</creatorcontrib><creatorcontrib>Kukreja, Rakesh C.</creatorcontrib><creatorcontrib>Sholley, Milton M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gill, Richard R.</au><au>Gbur, Jr, Charles J.</au><au>Fisher, Bernard J.</au><au>Hess, Michael L.</au><au>Fowler, III, Alpha A.</au><au>Kukreja, Rakesh C.</au><au>Sholley, Milton M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1998-12-01</date><risdate>1998</risdate><volume>30</volume><issue>12</issue><spage>2739</spage><epage>2749</epage><pages>2739-2749</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury, possibly via increased synthesis of heat shock proteins (HSPs). We hypothesized that heat shock preconditioning may protect human endothelial cells against oxidative damage. Cultured human umbilical vein endothelial cells (HUVEC) were subjected to heat shock (42°C, 1 h) and allowed to recover for 2 or 20 h, at which times the cells were oxidatively stressed for 1 h by exposing them to 100–200μmol/l of hydrogen peroxide (H2O2). Cellular damage was assessed immediately and 18 h later by morphology and release of lactate dehydrogenase (LDH). No protection of HUVEC was seen using the 2-hour recovery interval, but a significant protection (P<0.05) was observed after the 20-hour delay. Northern blot analysis at 1 and 2 h after heating showed induction of HSP-70 mRNA. Western blot analysis demonstrated a significant increase in HSP-72 protein after 2 as well as 20 h of recovery from heat shock, although the amounts of protein at the two times were not significantly different. Furthermore, no differences in the activity of the antioxidant enzyme catalase were observed between heated and unheated HUVEC at 2 and 20 h after heat preconditioning. Thus, heat shock preconditioning inducesdelayedprotection against oxidative injury in HUVEC, and the mechanism of protection appears to involve more than the expression of HSP-72 or activity of catalase.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>9990544</pmid><doi>10.1006/jmcc.1998.0837</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-2828 |
| ispartof | Journal of molecular and cellular cardiology, 1998-12, Vol.30 (12), p.2739-2749 |
| issn | 0022-2828 1095-8584 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69176925 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Blotting, Northern Blotting, Western Catalase - physiology Cell culture Cells, Cultured Dose-Response Relationship, Drug Endothelial cells Endothelium, Vascular - physiology Heat shock proteins Heat-Shock Proteins - pharmacology Heat-Shock Response - physiology HSP72 Heat-Shock Proteins Humans Hydrogen Peroxide - pharmacology L-Lactate Dehydrogenase - analysis Oxidative injury Oxidative Stress - physiology Preconditioning Temperature Time Factors Umbilical Veins - physiology |
| title | Heat Shock Provides Delayed Protection against Oxidative Injury in Cultured Human Umbilical Vein Endothelial Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T15%3A25%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=Heat%20Shock%20Provides%20Delayed%20Protection%20against%20Oxidative%20Injury%20in%20Cultured%20Human%20Umbilical%20Vein%20Endothelial%20Cells&rft.jtitle=Journal%20of%20molecular%20and%20cellular%20cardiology&rft.au=Gill,%20Richard%20R.&rft.date=1998-12-01&rft.volume=30&rft.issue=12&rft.spage=2739&rft.epage=2749&rft.pages=2739-2749&rft.issn=0022-2828&rft.eissn=1095-8584&rft_id=info:doi/10.1006/jmcc.1998.0837&rft_dat=%3Cproquest_cross%3E69176925%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=69176925&rft_id=info:pmid/9990544&rft_els_id=S0022282898908379&rfr_iscdi=true |