Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury
We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myoc...
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| Veröffentlicht in: | Stem cell research 2013-05, Vol.10 (3), p.301-312 |
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| creator | Arslan, Fatih Lai, Ruenn Chai Smeets, Mirjam B. Akeroyd, Lars Choo, Andre Aguor, Eissa N.E. Timmers, Leo van Rijen, Harold V. Doevendans, Pieter A. Pasterkamp, Gerard Lim, Sai Kiang de Kleijn, Dominique P. |
| description | We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myocardium, and could be ameliorated by proteins in exosomes. To test this hypothesis in vivo, mice (C57Bl6/J) underwent 30min ischemia, followed by reperfusion (I/R injury). Purified exosomes or saline was administered 5min before reperfusion. Exosomes reduced infarct size by 45% compared to saline treatment. Langendorff experiments revealed that intact but not lysed exosomes enhanced viability of the ischemic/reperfused myocardium. Exosome treated animals exhibited significant preservation of left ventricular geometry and contractile performance during 28days follow-up. Within an hour after reperfusion, exosome treatment increased levels of ATP and NADH, decreased oxidative stress, increased phosphorylated-Akt and phosphorylated-GSK-3β, and reduced phosphorylated-c-JNK in ischemic/reperfused hearts. Subsequently, both local and systemic inflammation were significantly reduced 24h after reperfusion. In conclusion, our study shows that intact exosomes restore bioenergetics, reduce oxidative stress and activate pro-survival signaling, thereby enhancing cardiac function and geometry after myocardial I/R injury. Hence, mesenchymal stem cell-derived exosomes are a potential adjuvant to reperfusion therapy for myocardial infarction.
► Therapeutic action of exosomes depend on their integrity and interaction with myocardial cells. ► Exosomes rapidly restore bioenergetics and reduce oxidative stress. ► Exosomes phosphorylate Akt/GSK3αβ pathway, and not ERK1/2 in vivo. ► Exosomes improve both short- and longterm cardiac function and geometry. |
| doi_str_mv | 10.1016/j.scr.2013.01.002 |
| format | Article |
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► Therapeutic action of exosomes depend on their integrity and interaction with myocardial cells. ► Exosomes rapidly restore bioenergetics and reduce oxidative stress. ► Exosomes phosphorylate Akt/GSK3αβ pathway, and not ERK1/2 in vivo. ► Exosomes improve both short- and longterm cardiac function and geometry.</description><identifier>ISSN: 1873-5061</identifier><identifier>EISSN: 1876-7753</identifier><identifier>DOI: 10.1016/j.scr.2013.01.002</identifier><identifier>PMID: 23399448</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Adenosine Triphosphate - metabolism ; AKT protein ; Animals ; Cell Survival ; Cells, Cultured ; Exosomes - metabolism ; Glycogen Synthase Kinase 3 - metabolism ; Glycogen Synthase Kinase 3 beta ; Heart - physiopathology ; Magnetic Resonance Imaging ; Male ; Mesenchymal Stromal Cells - cytology ; Mesenchymal Stromal Cells - metabolism ; Mice ; Mice, Inbred C57BL ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - physiopathology ; Myocardium - cytology ; Myocardium - metabolism ; Oxidative Stress ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Ventricular Remodeling</subject><ispartof>Stem cell research, 2013-05, Vol.10 (3), p.301-312</ispartof><rights>2013 Elsevier B.V.</rights><rights>Copyright © 2013 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-44e3033f322890f487e4f7ca8edc2b6e5e4008dfdc9697cc012527b9a410e9e3</citedby><cites>FETCH-LOGICAL-c386t-44e3033f322890f487e4f7ca8edc2b6e5e4008dfdc9697cc012527b9a410e9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1873506113000032$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23399448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arslan, Fatih</creatorcontrib><creatorcontrib>Lai, Ruenn Chai</creatorcontrib><creatorcontrib>Smeets, Mirjam B.</creatorcontrib><creatorcontrib>Akeroyd, Lars</creatorcontrib><creatorcontrib>Choo, Andre</creatorcontrib><creatorcontrib>Aguor, Eissa N.E.</creatorcontrib><creatorcontrib>Timmers, Leo</creatorcontrib><creatorcontrib>van Rijen, Harold V.</creatorcontrib><creatorcontrib>Doevendans, Pieter A.</creatorcontrib><creatorcontrib>Pasterkamp, Gerard</creatorcontrib><creatorcontrib>Lim, Sai Kiang</creatorcontrib><creatorcontrib>de Kleijn, Dominique P.</creatorcontrib><title>Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury</title><title>Stem cell research</title><addtitle>Stem Cell Res</addtitle><description>We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myocardium, and could be ameliorated by proteins in exosomes. To test this hypothesis in vivo, mice (C57Bl6/J) underwent 30min ischemia, followed by reperfusion (I/R injury). Purified exosomes or saline was administered 5min before reperfusion. Exosomes reduced infarct size by 45% compared to saline treatment. Langendorff experiments revealed that intact but not lysed exosomes enhanced viability of the ischemic/reperfused myocardium. Exosome treated animals exhibited significant preservation of left ventricular geometry and contractile performance during 28days follow-up. Within an hour after reperfusion, exosome treatment increased levels of ATP and NADH, decreased oxidative stress, increased phosphorylated-Akt and phosphorylated-GSK-3β, and reduced phosphorylated-c-JNK in ischemic/reperfused hearts. Subsequently, both local and systemic inflammation were significantly reduced 24h after reperfusion. In conclusion, our study shows that intact exosomes restore bioenergetics, reduce oxidative stress and activate pro-survival signaling, thereby enhancing cardiac function and geometry after myocardial I/R injury. Hence, mesenchymal stem cell-derived exosomes are a potential adjuvant to reperfusion therapy for myocardial infarction.
► Therapeutic action of exosomes depend on their integrity and interaction with myocardial cells. ► Exosomes rapidly restore bioenergetics and reduce oxidative stress. ► Exosomes phosphorylate Akt/GSK3αβ pathway, and not ERK1/2 in vivo. ► Exosomes improve both short- and longterm cardiac function and geometry.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Exosomes - metabolism</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta</subject><subject>Heart - physiopathology</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Mesenchymal Stromal Cells - cytology</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - physiopathology</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Oxidative Stress</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Ventricular Remodeling</subject><issn>1873-5061</issn><issn>1876-7753</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUstuEzEUHSEQLYUPYIO8ZMFM_JinWEUVj4oiusjecuwzxGFmHGwndL62v1K3CYgVrO7V1Xlc3Xuy7DWjBaOsXmyLoH3BKRMFZQWl_El2ztqmzpumEk8fe5FXtGZn2YsQtpRWHW_58-yMC9F1ZdmeZ3dfETDpzTyqgYSIkWgMQ27g7QGG4NYFNyIQO2kPFUCWqxsy4IAhvCMGp6G7tUbFxEgSHiEQNRmidJqoCHJzJb4slj8i2am4-aVmEh3BtFGTBhlnp5U3NrkfrFrbwcb5kb3zyWSKRJkDfLLwGJ3BYKfvRPUR_m-mDXqD0aqFxw6-3wfrprTxdu_nl9mzXg0Br071Ilt9_LC6_Jxff_t0dbm8zrVo65iXJQQVohectx3ty7ZB2TdatTCar2tUKCltTW90V3eN1pTxijfrTpWMooO4yN4eZXfe_dwjRDmmpdIl1QS3D5JVlDYt4w3_P1TwsqtZx-oEZUeo9i4Ej17uvB2VnyWj8iEBcitTAuRDAiRlMiUgcd6c5PfrEeYP4_fLE-D9EZBeiIOFTxI2RQDGeugojbP_kL8HOXzHUQ</recordid><startdate>201305</startdate><enddate>201305</enddate><creator>Arslan, Fatih</creator><creator>Lai, Ruenn Chai</creator><creator>Smeets, Mirjam B.</creator><creator>Akeroyd, Lars</creator><creator>Choo, Andre</creator><creator>Aguor, Eissa N.E.</creator><creator>Timmers, Leo</creator><creator>van Rijen, Harold V.</creator><creator>Doevendans, Pieter A.</creator><creator>Pasterkamp, Gerard</creator><creator>Lim, Sai Kiang</creator><creator>de Kleijn, Dominique P.</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201305</creationdate><title>Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury</title><author>Arslan, Fatih ; Lai, Ruenn Chai ; Smeets, Mirjam B. ; Akeroyd, Lars ; Choo, Andre ; Aguor, Eissa N.E. ; Timmers, Leo ; van Rijen, Harold V. ; Doevendans, Pieter A. ; Pasterkamp, Gerard ; Lim, Sai Kiang ; de Kleijn, Dominique P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-44e3033f322890f487e4f7ca8edc2b6e5e4008dfdc9697cc012527b9a410e9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Exosomes - metabolism</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta</topic><topic>Heart - physiopathology</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Mesenchymal Stromal Cells - cytology</topic><topic>Mesenchymal Stromal Cells - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - physiopathology</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Oxidative Stress</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arslan, Fatih</creatorcontrib><creatorcontrib>Lai, Ruenn Chai</creatorcontrib><creatorcontrib>Smeets, Mirjam B.</creatorcontrib><creatorcontrib>Akeroyd, Lars</creatorcontrib><creatorcontrib>Choo, Andre</creatorcontrib><creatorcontrib>Aguor, Eissa N.E.</creatorcontrib><creatorcontrib>Timmers, Leo</creatorcontrib><creatorcontrib>van Rijen, Harold V.</creatorcontrib><creatorcontrib>Doevendans, Pieter A.</creatorcontrib><creatorcontrib>Pasterkamp, Gerard</creatorcontrib><creatorcontrib>Lim, Sai Kiang</creatorcontrib><creatorcontrib>de Kleijn, Dominique P.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Stem cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arslan, Fatih</au><au>Lai, Ruenn Chai</au><au>Smeets, Mirjam B.</au><au>Akeroyd, Lars</au><au>Choo, Andre</au><au>Aguor, Eissa N.E.</au><au>Timmers, Leo</au><au>van Rijen, Harold V.</au><au>Doevendans, Pieter A.</au><au>Pasterkamp, Gerard</au><au>Lim, Sai Kiang</au><au>de Kleijn, Dominique P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury</atitle><jtitle>Stem cell research</jtitle><addtitle>Stem Cell Res</addtitle><date>2013-05</date><risdate>2013</risdate><volume>10</volume><issue>3</issue><spage>301</spage><epage>312</epage><pages>301-312</pages><issn>1873-5061</issn><eissn>1876-7753</eissn><abstract>We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myocardium, and could be ameliorated by proteins in exosomes. To test this hypothesis in vivo, mice (C57Bl6/J) underwent 30min ischemia, followed by reperfusion (I/R injury). Purified exosomes or saline was administered 5min before reperfusion. Exosomes reduced infarct size by 45% compared to saline treatment. Langendorff experiments revealed that intact but not lysed exosomes enhanced viability of the ischemic/reperfused myocardium. Exosome treated animals exhibited significant preservation of left ventricular geometry and contractile performance during 28days follow-up. Within an hour after reperfusion, exosome treatment increased levels of ATP and NADH, decreased oxidative stress, increased phosphorylated-Akt and phosphorylated-GSK-3β, and reduced phosphorylated-c-JNK in ischemic/reperfused hearts. Subsequently, both local and systemic inflammation were significantly reduced 24h after reperfusion. In conclusion, our study shows that intact exosomes restore bioenergetics, reduce oxidative stress and activate pro-survival signaling, thereby enhancing cardiac function and geometry after myocardial I/R injury. Hence, mesenchymal stem cell-derived exosomes are a potential adjuvant to reperfusion therapy for myocardial infarction.
► Therapeutic action of exosomes depend on their integrity and interaction with myocardial cells. ► Exosomes rapidly restore bioenergetics and reduce oxidative stress. ► Exosomes phosphorylate Akt/GSK3αβ pathway, and not ERK1/2 in vivo. ► Exosomes improve both short- and longterm cardiac function and geometry.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>23399448</pmid><doi>10.1016/j.scr.2013.01.002</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Triphosphate - metabolism AKT protein Animals Cell Survival Cells, Cultured Exosomes - metabolism Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Heart - physiopathology Magnetic Resonance Imaging Male Mesenchymal Stromal Cells - cytology Mesenchymal Stromal Cells - metabolism Mice Mice, Inbred C57BL Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - physiopathology Myocardium - cytology Myocardium - metabolism Oxidative Stress Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Ventricular Remodeling |
| title | Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury |
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