Stromal cell-derived factor-1 retention and cardioprotection for ischemic myocardium
Stromal cell-derived factor-1 (SDF-1) is a chemoattractant of stem/progenitor cells, and several studies have shown that SDF-1 may improve ventricular function after infarction. SDF-1 is cleaved by proteases including matrix metalloproteinase-2 (MMP-2) and CD26/dipeptidylpeptidase-4 (DPP-4), which a...
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| Veröffentlicht in: | Circulation. Heart failure 2011-07, Vol.4 (4), p.509-518 |
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| container_title | Circulation. Heart failure |
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| creator | Kanki, Sachiko Segers, Vincent F M Wu, Weitao Kakkar, Rahul Gannon, Joseph Sys, Stanislas U Sandrasagra, Anthony Lee, Richard T |
| description | Stromal cell-derived factor-1 (SDF-1) is a chemoattractant of stem/progenitor cells, and several studies have shown that SDF-1 may improve ventricular function after infarction. SDF-1 is cleaved by proteases including matrix metalloproteinase-2 (MMP-2) and CD26/dipeptidylpeptidase-4 (DPP-4), which are activated in injured tissues.
We investigated the biodistribution and functional roles of SDF-1 in experimental ischemia/reperfusion injury in rats. Radiolabeled SDF-1 given by intracoronary injection was selectively concentrated in ischemic myocardium. The enhanced uptake of SDF-1 in ischemic myocardium was not mediated by its receptor, CXCR4. Mass spectrometry and Western analyses showed that SDF-1 was cleaved by DPP-4 in plasma and myocardium, whereas a bioengineered MMP-2/DPP-4-resistant form of SDF-1, SSDF-1(S4V), was highly stable. A single dose of SSDF-1(S4V) exhibited greater potency for cardioprotection than wild-type SDF-1. SSDF-1(S4V) improved cardiac function in rats even after a 3-hour ischemic period.
These results show that a single dose of protease-resistant SSDF-1(S4V) after myocardial infarction leads to dramatic improvement in angiogenesis and ventricular function even 3 hours after the onset of ischemia, revealing a simple, clinically feasible approach to prevention of heart failure. |
| doi_str_mv | 10.1161/circheartfailure.110.960302 |
| format | Article |
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We investigated the biodistribution and functional roles of SDF-1 in experimental ischemia/reperfusion injury in rats. Radiolabeled SDF-1 given by intracoronary injection was selectively concentrated in ischemic myocardium. The enhanced uptake of SDF-1 in ischemic myocardium was not mediated by its receptor, CXCR4. Mass spectrometry and Western analyses showed that SDF-1 was cleaved by DPP-4 in plasma and myocardium, whereas a bioengineered MMP-2/DPP-4-resistant form of SDF-1, SSDF-1(S4V), was highly stable. A single dose of SSDF-1(S4V) exhibited greater potency for cardioprotection than wild-type SDF-1. SSDF-1(S4V) improved cardiac function in rats even after a 3-hour ischemic period.
These results show that a single dose of protease-resistant SSDF-1(S4V) after myocardial infarction leads to dramatic improvement in angiogenesis and ventricular function even 3 hours after the onset of ischemia, revealing a simple, clinically feasible approach to prevention of heart failure.</description><identifier>ISSN: 1941-3289</identifier><identifier>EISSN: 1941-3297</identifier><identifier>DOI: 10.1161/circheartfailure.110.960302</identifier><identifier>PMID: 21606214</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Capillaries - drug effects ; Chemokine CXCL12 - administration & dosage ; Chemokine CXCL12 - pharmacology ; Chemokine CXCL12 - therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Heart - drug effects ; Heart - physiology ; Heart Failure - prevention & control ; Injections, Intra-Arterial ; Matrix Metalloproteinase 2 - metabolism ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Myocardium - metabolism ; Neovascularization, Physiologic - drug effects ; Neovascularization, Physiologic - physiology ; Rats ; Receptors, CXCR4 - metabolism ; Treatment Outcome</subject><ispartof>Circulation. Heart failure, 2011-07, Vol.4 (4), p.509-518</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-21198ca3f291b6478188d859f2c9081424b0ee3364766242828ede4c977712503</citedby><cites>FETCH-LOGICAL-c439t-21198ca3f291b6478188d859f2c9081424b0ee3364766242828ede4c977712503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21606214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanki, Sachiko</creatorcontrib><creatorcontrib>Segers, Vincent F M</creatorcontrib><creatorcontrib>Wu, Weitao</creatorcontrib><creatorcontrib>Kakkar, Rahul</creatorcontrib><creatorcontrib>Gannon, Joseph</creatorcontrib><creatorcontrib>Sys, Stanislas U</creatorcontrib><creatorcontrib>Sandrasagra, Anthony</creatorcontrib><creatorcontrib>Lee, Richard T</creatorcontrib><title>Stromal cell-derived factor-1 retention and cardioprotection for ischemic myocardium</title><title>Circulation. Heart failure</title><addtitle>Circ Heart Fail</addtitle><description>Stromal cell-derived factor-1 (SDF-1) is a chemoattractant of stem/progenitor cells, and several studies have shown that SDF-1 may improve ventricular function after infarction. SDF-1 is cleaved by proteases including matrix metalloproteinase-2 (MMP-2) and CD26/dipeptidylpeptidase-4 (DPP-4), which are activated in injured tissues.
We investigated the biodistribution and functional roles of SDF-1 in experimental ischemia/reperfusion injury in rats. Radiolabeled SDF-1 given by intracoronary injection was selectively concentrated in ischemic myocardium. The enhanced uptake of SDF-1 in ischemic myocardium was not mediated by its receptor, CXCR4. Mass spectrometry and Western analyses showed that SDF-1 was cleaved by DPP-4 in plasma and myocardium, whereas a bioengineered MMP-2/DPP-4-resistant form of SDF-1, SSDF-1(S4V), was highly stable. A single dose of SSDF-1(S4V) exhibited greater potency for cardioprotection than wild-type SDF-1. SSDF-1(S4V) improved cardiac function in rats even after a 3-hour ischemic period.
These results show that a single dose of protease-resistant SSDF-1(S4V) after myocardial infarction leads to dramatic improvement in angiogenesis and ventricular function even 3 hours after the onset of ischemia, revealing a simple, clinically feasible approach to prevention of heart failure.</description><subject>Animals</subject><subject>Capillaries - drug effects</subject><subject>Chemokine CXCL12 - administration & dosage</subject><subject>Chemokine CXCL12 - pharmacology</subject><subject>Chemokine CXCL12 - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Heart - drug effects</subject><subject>Heart - physiology</subject><subject>Heart Failure - prevention & control</subject><subject>Injections, Intra-Arterial</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Rats</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Treatment Outcome</subject><issn>1941-3289</issn><issn>1941-3297</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kFFrwjAUhcPYmM7tL4zCnutyk7RN2JMUnYIwcPpcYnLLMlojaRz471d18-kezr3f5XAIeQE6Bsjh1bhgvlCHWGvXHAL2Lh2rnHLKbsgQlICUM1XcXrVUA_LQdd-U5izL1D0ZMMh7DWJI1p8x-FY3icGmSS0G94M2qbWJPqSQBIy4i87vEr2zidHBOr8PPqI5m7UPiev6NK0zSXv054ND-0juat10-PQ3R2Qzm67Lebr8eF-Uk2VqBFcxZQBKGs1rpmCbi0KClFZmqmZGUQmCiS1F5Lxf5TkTTDKJFoVRRVEAyygfkbfLXxN81wWsq31wrQ7HCmh16qoqF6tyPp2s1rPJYrlZTXuXVpeuevr5Qu8P2xbtlf0vh_8CD6Bo5Q</recordid><startdate>201107</startdate><enddate>201107</enddate><creator>Kanki, Sachiko</creator><creator>Segers, Vincent F M</creator><creator>Wu, Weitao</creator><creator>Kakkar, Rahul</creator><creator>Gannon, Joseph</creator><creator>Sys, Stanislas U</creator><creator>Sandrasagra, Anthony</creator><creator>Lee, Richard T</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>201107</creationdate><title>Stromal cell-derived factor-1 retention and cardioprotection for ischemic myocardium</title><author>Kanki, Sachiko ; Segers, Vincent F M ; Wu, Weitao ; Kakkar, Rahul ; Gannon, Joseph ; Sys, Stanislas U ; Sandrasagra, Anthony ; Lee, Richard T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-21198ca3f291b6478188d859f2c9081424b0ee3364766242828ede4c977712503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Capillaries - drug effects</topic><topic>Chemokine CXCL12 - administration & dosage</topic><topic>Chemokine CXCL12 - pharmacology</topic><topic>Chemokine CXCL12 - therapeutic use</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Heart - drug effects</topic><topic>Heart - physiology</topic><topic>Heart Failure - prevention & control</topic><topic>Injections, Intra-Arterial</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Rats</topic><topic>Receptors, CXCR4 - metabolism</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kanki, Sachiko</creatorcontrib><creatorcontrib>Segers, Vincent F M</creatorcontrib><creatorcontrib>Wu, Weitao</creatorcontrib><creatorcontrib>Kakkar, Rahul</creatorcontrib><creatorcontrib>Gannon, Joseph</creatorcontrib><creatorcontrib>Sys, Stanislas U</creatorcontrib><creatorcontrib>Sandrasagra, Anthony</creatorcontrib><creatorcontrib>Lee, Richard T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Circulation. Heart failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanki, Sachiko</au><au>Segers, Vincent F M</au><au>Wu, Weitao</au><au>Kakkar, Rahul</au><au>Gannon, Joseph</au><au>Sys, Stanislas U</au><au>Sandrasagra, Anthony</au><au>Lee, Richard T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stromal cell-derived factor-1 retention and cardioprotection for ischemic myocardium</atitle><jtitle>Circulation. Heart failure</jtitle><addtitle>Circ Heart Fail</addtitle><date>2011-07</date><risdate>2011</risdate><volume>4</volume><issue>4</issue><spage>509</spage><epage>518</epage><pages>509-518</pages><issn>1941-3289</issn><eissn>1941-3297</eissn><abstract>Stromal cell-derived factor-1 (SDF-1) is a chemoattractant of stem/progenitor cells, and several studies have shown that SDF-1 may improve ventricular function after infarction. SDF-1 is cleaved by proteases including matrix metalloproteinase-2 (MMP-2) and CD26/dipeptidylpeptidase-4 (DPP-4), which are activated in injured tissues.
We investigated the biodistribution and functional roles of SDF-1 in experimental ischemia/reperfusion injury in rats. Radiolabeled SDF-1 given by intracoronary injection was selectively concentrated in ischemic myocardium. The enhanced uptake of SDF-1 in ischemic myocardium was not mediated by its receptor, CXCR4. Mass spectrometry and Western analyses showed that SDF-1 was cleaved by DPP-4 in plasma and myocardium, whereas a bioengineered MMP-2/DPP-4-resistant form of SDF-1, SSDF-1(S4V), was highly stable. A single dose of SSDF-1(S4V) exhibited greater potency for cardioprotection than wild-type SDF-1. SSDF-1(S4V) improved cardiac function in rats even after a 3-hour ischemic period.
These results show that a single dose of protease-resistant SSDF-1(S4V) after myocardial infarction leads to dramatic improvement in angiogenesis and ventricular function even 3 hours after the onset of ischemia, revealing a simple, clinically feasible approach to prevention of heart failure.</abstract><cop>United States</cop><pmid>21606214</pmid><doi>10.1161/circheartfailure.110.960302</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation. Heart failure, 2011-07, Vol.4 (4), p.509-518 |
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| source | MEDLINE; American Heart Association; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Capillaries - drug effects Chemokine CXCL12 - administration & dosage Chemokine CXCL12 - pharmacology Chemokine CXCL12 - therapeutic use Disease Models, Animal Dose-Response Relationship, Drug Heart - drug effects Heart - physiology Heart Failure - prevention & control Injections, Intra-Arterial Matrix Metalloproteinase 2 - metabolism Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - metabolism Myocardium - metabolism Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Rats Receptors, CXCR4 - metabolism Treatment Outcome |
| title | Stromal cell-derived factor-1 retention and cardioprotection for ischemic myocardium |
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