Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction
During acute myocardial infarction (AMI), ischemia leads to necrotic areas surrounded by border zones of reversibly damaged cardiomyocytes, showing membrane flip-flop. During reperfusion type IIA secretory phopholipase A₂ (sPLA₂-IIA) induces direct cell-toxicity and facilitates binding of other infl...
Gespeichert in:
| Veröffentlicht in: | Apoptosis (London) 2009-06, Vol.14 (6), p.753-763 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 763 |
|---|---|
| container_issue | 6 |
| container_start_page | 753 |
| container_title | Apoptosis (London) |
| container_volume | 14 |
| creator | van Dijk, Annemieke Krijnen, Paul A. J Vermond, Rob A Pronk, Amanda Spreeuwenberg, Marieke Visser, Frans C Berney, Richard Paulus, Walter J Hack, C. Erik van Milligen, Florine J Niessen, Hans W. M |
| description | During acute myocardial infarction (AMI), ischemia leads to necrotic areas surrounded by border zones of reversibly damaged cardiomyocytes, showing membrane flip-flop. During reperfusion type IIA secretory phopholipase A₂ (sPLA₂-IIA) induces direct cell-toxicity and facilitates binding of other inflammatory mediators on these cardiomyocytes. Therefore, we hypothesized that the specific sPLA₂-IIA-inhibitor PX-18 would reduce cardiomyocyte death and infarct size in vivo. Wistar rats were treated with PX-18 starting minutes after reperfusion, and at day 1 and 2 post AMI. After 28 days hearts were analyzed. Furthermore, the effect of PX-18 on membrane flip-flop and apoptosis was investigated in vitro. PX-18 significantly inhibited sPLA₂-IIA activity and reduced infarct size (reduction 73 ± 9%, P < 0.05), compared to the vehicle-treated group, without impairing wound healing. In vitro, PX-18 significantly reduced reversible membrane flip-flop and apoptosis in cardiomyocytes. However, no sPLA₂-IIA activity could be detected, suggesting that PX-18 also exerted a protective effect independent of sPLA₂-IIA. In conclusion, PX-18 is a potent therapeutic to reduce infarct size by inhibiting sPLA₂-IIA, and possibly also by inhibiting apoptosis of cardiomyocytes in a sPLA₂-IIA independent manner. |
| doi_str_mv | 10.1007/s10495-009-0350-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_236155925</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1895884441</sourcerecordid><originalsourceid>FETCH-LOGICAL-c351x-21941c2bd76f99ebe4c139e43e73c13f0a49981f7fde9152b995702c16ac959e3</originalsourceid><addsrcrecordid>eNp9UE1r3DAQFaWlSdP-gF5a0bvbGcmyreMS-hEI9NAGehOyPMo67FqOZMP6mp_aX1IZL-TWg9Dw5n0Mj7H3CJ8RoP6SEEqtCgBdgFRQnF6wS1S1LKpa_XmZZ1lB0WCjLtiblB4AQDayfM0uUJcCmwov2ePNsO_bfurDwIPn0zISFzueyEWaQlz4uA8pv0M_2kR89_fpiUfqZkeJd2Sn_apyNnZ9OC7BLVPG-4FbN0_EV2Rd2UPGvI1ujXnLXnl7SPTu_F-xu29ff1__KG5_fr-53t0WTio8FSLfiE60XV15raml0qHUVEqqZZ482FLrBn3tO9KoRKu1qkE4rKzTSpO8Yp823zGGx5nSZB7CHIccaYSsUCktVCbhRnIxpBTJmzH2RxsXg2DWjs3Wsckdm7Vjc8qaD2fjuT1S96w4l5oJYiOkvBruKT4n_8_14ybyNhh7H_tk7n4JQAlYybKCUv4DU9iSvg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>236155925</pqid></control><display><type>article</type><title>Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>van Dijk, Annemieke ; Krijnen, Paul A. J ; Vermond, Rob A ; Pronk, Amanda ; Spreeuwenberg, Marieke ; Visser, Frans C ; Berney, Richard ; Paulus, Walter J ; Hack, C. Erik ; van Milligen, Florine J ; Niessen, Hans W. M</creator><creatorcontrib>van Dijk, Annemieke ; Krijnen, Paul A. J ; Vermond, Rob A ; Pronk, Amanda ; Spreeuwenberg, Marieke ; Visser, Frans C ; Berney, Richard ; Paulus, Walter J ; Hack, C. Erik ; van Milligen, Florine J ; Niessen, Hans W. M</creatorcontrib><description>During acute myocardial infarction (AMI), ischemia leads to necrotic areas surrounded by border zones of reversibly damaged cardiomyocytes, showing membrane flip-flop. During reperfusion type IIA secretory phopholipase A₂ (sPLA₂-IIA) induces direct cell-toxicity and facilitates binding of other inflammatory mediators on these cardiomyocytes. Therefore, we hypothesized that the specific sPLA₂-IIA-inhibitor PX-18 would reduce cardiomyocyte death and infarct size in vivo. Wistar rats were treated with PX-18 starting minutes after reperfusion, and at day 1 and 2 post AMI. After 28 days hearts were analyzed. Furthermore, the effect of PX-18 on membrane flip-flop and apoptosis was investigated in vitro. PX-18 significantly inhibited sPLA₂-IIA activity and reduced infarct size (reduction 73 ± 9%, P < 0.05), compared to the vehicle-treated group, without impairing wound healing. In vitro, PX-18 significantly reduced reversible membrane flip-flop and apoptosis in cardiomyocytes. However, no sPLA₂-IIA activity could be detected, suggesting that PX-18 also exerted a protective effect independent of sPLA₂-IIA. In conclusion, PX-18 is a potent therapeutic to reduce infarct size by inhibiting sPLA₂-IIA, and possibly also by inhibiting apoptosis of cardiomyocytes in a sPLA₂-IIA independent manner.</description><identifier>ISSN: 1360-8185</identifier><identifier>EISSN: 1573-675X</identifier><identifier>DOI: 10.1007/s10495-009-0350-x</identifier><identifier>PMID: 19421861</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Animals ; Apoptosis - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Caspase 3 - metabolism ; Cell Biology ; Cell Membrane - drug effects ; Cell Membrane - enzymology ; Cell Movement - drug effects ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Group II Phospholipases A2 - antagonists & inhibitors ; Heart Function Tests ; Immunohistochemistry ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - enzymology ; Myocardial infarction ; Myocardial Infarction - enzymology ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - enzymology ; Neutrophils - cytology ; Neutrophils - drug effects ; Neutrophils - enzymology ; Oncology ; Original Paper ; Rats ; Rats, Wistar ; Simvastatin - pharmacology ; Solubility - drug effects ; Virology</subject><ispartof>Apoptosis (London), 2009-06, Vol.14 (6), p.753-763</ispartof><rights>The Author(s) 2009</rights><rights>Springer Science+Business Media, LLC 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c351x-21941c2bd76f99ebe4c139e43e73c13f0a49981f7fde9152b995702c16ac959e3</citedby><cites>FETCH-LOGICAL-c351x-21941c2bd76f99ebe4c139e43e73c13f0a49981f7fde9152b995702c16ac959e3</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/s10495-009-0350-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10495-009-0350-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19421861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Dijk, Annemieke</creatorcontrib><creatorcontrib>Krijnen, Paul A. J</creatorcontrib><creatorcontrib>Vermond, Rob A</creatorcontrib><creatorcontrib>Pronk, Amanda</creatorcontrib><creatorcontrib>Spreeuwenberg, Marieke</creatorcontrib><creatorcontrib>Visser, Frans C</creatorcontrib><creatorcontrib>Berney, Richard</creatorcontrib><creatorcontrib>Paulus, Walter J</creatorcontrib><creatorcontrib>Hack, C. Erik</creatorcontrib><creatorcontrib>van Milligen, Florine J</creatorcontrib><creatorcontrib>Niessen, Hans W. M</creatorcontrib><title>Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction</title><title>Apoptosis (London)</title><addtitle>Apoptosis</addtitle><addtitle>Apoptosis</addtitle><description>During acute myocardial infarction (AMI), ischemia leads to necrotic areas surrounded by border zones of reversibly damaged cardiomyocytes, showing membrane flip-flop. During reperfusion type IIA secretory phopholipase A₂ (sPLA₂-IIA) induces direct cell-toxicity and facilitates binding of other inflammatory mediators on these cardiomyocytes. Therefore, we hypothesized that the specific sPLA₂-IIA-inhibitor PX-18 would reduce cardiomyocyte death and infarct size in vivo. Wistar rats were treated with PX-18 starting minutes after reperfusion, and at day 1 and 2 post AMI. After 28 days hearts were analyzed. Furthermore, the effect of PX-18 on membrane flip-flop and apoptosis was investigated in vitro. PX-18 significantly inhibited sPLA₂-IIA activity and reduced infarct size (reduction 73 ± 9%, P < 0.05), compared to the vehicle-treated group, without impairing wound healing. In vitro, PX-18 significantly reduced reversible membrane flip-flop and apoptosis in cardiomyocytes. However, no sPLA₂-IIA activity could be detected, suggesting that PX-18 also exerted a protective effect independent of sPLA₂-IIA. In conclusion, PX-18 is a potent therapeutic to reduce infarct size by inhibiting sPLA₂-IIA, and possibly also by inhibiting apoptosis of cardiomyocytes in a sPLA₂-IIA independent manner.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Biology</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - enzymology</subject><subject>Cell Movement - drug effects</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Group II Phospholipases A2 - antagonists & inhibitors</subject><subject>Heart Function Tests</subject><subject>Immunohistochemistry</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - enzymology</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - enzymology</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Simvastatin - pharmacology</subject><subject>Solubility - drug effects</subject><subject>Virology</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9UE1r3DAQFaWlSdP-gF5a0bvbGcmyreMS-hEI9NAGehOyPMo67FqOZMP6mp_aX1IZL-TWg9Dw5n0Mj7H3CJ8RoP6SEEqtCgBdgFRQnF6wS1S1LKpa_XmZZ1lB0WCjLtiblB4AQDayfM0uUJcCmwov2ePNsO_bfurDwIPn0zISFzueyEWaQlz4uA8pv0M_2kR89_fpiUfqZkeJd2Sn_apyNnZ9OC7BLVPG-4FbN0_EV2Rd2UPGvI1ujXnLXnl7SPTu_F-xu29ff1__KG5_fr-53t0WTio8FSLfiE60XV15raml0qHUVEqqZZ482FLrBn3tO9KoRKu1qkE4rKzTSpO8Yp823zGGx5nSZB7CHIccaYSsUCktVCbhRnIxpBTJmzH2RxsXg2DWjs3Wsckdm7Vjc8qaD2fjuT1S96w4l5oJYiOkvBruKT4n_8_14ybyNhh7H_tk7n4JQAlYybKCUv4DU9iSvg</recordid><startdate>200906</startdate><enddate>200906</enddate><creator>van Dijk, Annemieke</creator><creator>Krijnen, Paul A. J</creator><creator>Vermond, Rob A</creator><creator>Pronk, Amanda</creator><creator>Spreeuwenberg, Marieke</creator><creator>Visser, Frans C</creator><creator>Berney, Richard</creator><creator>Paulus, Walter J</creator><creator>Hack, C. Erik</creator><creator>van Milligen, Florine J</creator><creator>Niessen, Hans W. M</creator><general>Boston : Springer US</general><general>Springer US</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>C6C</scope><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>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</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>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope></search><sort><creationdate>200906</creationdate><title>Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction</title><author>van Dijk, Annemieke ; Krijnen, Paul A. J ; Vermond, Rob A ; Pronk, Amanda ; Spreeuwenberg, Marieke ; Visser, Frans C ; Berney, Richard ; Paulus, Walter J ; Hack, C. Erik ; van Milligen, Florine J ; Niessen, Hans W. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c351x-21941c2bd76f99ebe4c139e43e73c13f0a49981f7fde9152b995702c16ac959e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Biology</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - enzymology</topic><topic>Cell Movement - drug effects</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Group II Phospholipases A2 - antagonists & inhibitors</topic><topic>Heart Function Tests</topic><topic>Immunohistochemistry</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - enzymology</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - enzymology</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Simvastatin - pharmacology</topic><topic>Solubility - drug effects</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Dijk, Annemieke</creatorcontrib><creatorcontrib>Krijnen, Paul A. J</creatorcontrib><creatorcontrib>Vermond, Rob A</creatorcontrib><creatorcontrib>Pronk, Amanda</creatorcontrib><creatorcontrib>Spreeuwenberg, Marieke</creatorcontrib><creatorcontrib>Visser, Frans C</creatorcontrib><creatorcontrib>Berney, Richard</creatorcontrib><creatorcontrib>Paulus, Walter J</creatorcontrib><creatorcontrib>Hack, C. Erik</creatorcontrib><creatorcontrib>van Milligen, Florine J</creatorcontrib><creatorcontrib>Niessen, Hans W. M</creatorcontrib><collection>AGRIS</collection><collection>Springer Nature OA Free Journals</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</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 Basic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Dijk, Annemieke</au><au>Krijnen, Paul A. J</au><au>Vermond, Rob A</au><au>Pronk, Amanda</au><au>Spreeuwenberg, Marieke</au><au>Visser, Frans C</au><au>Berney, Richard</au><au>Paulus, Walter J</au><au>Hack, C. Erik</au><au>van Milligen, Florine J</au><au>Niessen, Hans W. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2009-06</date><risdate>2009</risdate><volume>14</volume><issue>6</issue><spage>753</spage><epage>763</epage><pages>753-763</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>During acute myocardial infarction (AMI), ischemia leads to necrotic areas surrounded by border zones of reversibly damaged cardiomyocytes, showing membrane flip-flop. During reperfusion type IIA secretory phopholipase A₂ (sPLA₂-IIA) induces direct cell-toxicity and facilitates binding of other inflammatory mediators on these cardiomyocytes. Therefore, we hypothesized that the specific sPLA₂-IIA-inhibitor PX-18 would reduce cardiomyocyte death and infarct size in vivo. Wistar rats were treated with PX-18 starting minutes after reperfusion, and at day 1 and 2 post AMI. After 28 days hearts were analyzed. Furthermore, the effect of PX-18 on membrane flip-flop and apoptosis was investigated in vitro. PX-18 significantly inhibited sPLA₂-IIA activity and reduced infarct size (reduction 73 ± 9%, P < 0.05), compared to the vehicle-treated group, without impairing wound healing. In vitro, PX-18 significantly reduced reversible membrane flip-flop and apoptosis in cardiomyocytes. However, no sPLA₂-IIA activity could be detected, suggesting that PX-18 also exerted a protective effect independent of sPLA₂-IIA. In conclusion, PX-18 is a potent therapeutic to reduce infarct size by inhibiting sPLA₂-IIA, and possibly also by inhibiting apoptosis of cardiomyocytes in a sPLA₂-IIA independent manner.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>19421861</pmid><doi>10.1007/s10495-009-0350-x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1360-8185 |
| ispartof | Apoptosis (London), 2009-06, Vol.14 (6), p.753-763 |
| issn | 1360-8185 1573-675X |
| language | eng |
| recordid | cdi_proquest_journals_236155925 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Apoptosis - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research Caspase 3 - metabolism Cell Biology Cell Membrane - drug effects Cell Membrane - enzymology Cell Movement - drug effects Disease Models, Animal Enzyme Inhibitors - pharmacology Group II Phospholipases A2 - antagonists & inhibitors Heart Function Tests Immunohistochemistry Macrophages - cytology Macrophages - drug effects Macrophages - enzymology Myocardial infarction Myocardial Infarction - enzymology Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - enzymology Neutrophils - cytology Neutrophils - drug effects Neutrophils - enzymology Oncology Original Paper Rats Rats, Wistar Simvastatin - pharmacology Solubility - drug effects Virology |
| title | Inhibition of type 2A secretory phospholipase A₂ reduces death of cardiomyocytes in acute myocardial infarction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T03%3A00%3A26IST&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=Inhibition%20of%20type%202A%20secretory%20phospholipase%20A%E2%82%82%20reduces%20death%20of%20cardiomyocytes%20in%20acute%20myocardial%20infarction&rft.jtitle=Apoptosis%20(London)&rft.au=van%20Dijk,%20Annemieke&rft.date=2009-06&rft.volume=14&rft.issue=6&rft.spage=753&rft.epage=763&rft.pages=753-763&rft.issn=1360-8185&rft.eissn=1573-675X&rft_id=info:doi/10.1007/s10495-009-0350-x&rft_dat=%3Cproquest_cross%3E1895884441%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=236155925&rft_id=info:pmid/19421861&rfr_iscdi=true |