Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury
Background/Aims: Recent studies have indicated that exosomes play an important role in adipose-derived stem cell (ADSC) transplant-mediated ischaemic heart disease therapy. However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched wi...
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| Veröffentlicht in: | Cellular Physiology and Biochemistry 2017-01, Vol.44 (6), p.2105-2116 |
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| description | Background/Aims: Recent studies have indicated that exosomes play an important role in adipose-derived stem cell (ADSC) transplant-mediated ischaemic heart disease therapy. However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-126 have a more protective effect on acute myocardial infarction (AMI). Methods: Exosomes were characterized by transmission electron microscopy, and the exosome particles were further examined using nanoparticle tracking analyses. A rat model of myocardial infarction and in vitro model of hypoxia-induced H9c2 myocardial cell injury were established to study the protective mechanism of exosomes from miR-126-overexpressing ADSCs. Results: The in vitro results showed that exosomes derived from miR-126-overexpressing ADSCs decreased H9c2 myocardial cell injury by reducing inflammation factor expression during hypoxia induction. The miR-126-enriched exosomes also decreased the expression of fibrosis-related proteins of H9c2 cells under hypoxic conditions. Matrigel® and Transwell® assays showed that miR-126-enriched exosomes significantly promoted microvascular generation and migration, respectively. In vivo studies confirmed that exosomes derived from ADSCs significantly decreased the myocardial injury area of infarction, especially after miR-126-enriched exosome treatment. Cardiac fibrosis and inflammatory cytokine expression were also decreased after treatment with miR-126-enriched exosomes. However, blood vessel formation was promoted in the infarction region of AMI rats. Conclusions: The results suggested that the expression of miR-126-enhanced ADSC-derived exosomes prevented myocardial damage by protecting myocardial cells from apoptosis, inflammation, fibrosis, and increased angiogenesis. |
| doi_str_mv | 10.1159/000485949 |
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However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-126 have a more protective effect on acute myocardial infarction (AMI). Methods: Exosomes were characterized by transmission electron microscopy, and the exosome particles were further examined using nanoparticle tracking analyses. A rat model of myocardial infarction and in vitro model of hypoxia-induced H9c2 myocardial cell injury were established to study the protective mechanism of exosomes from miR-126-overexpressing ADSCs. Results: The in vitro results showed that exosomes derived from miR-126-overexpressing ADSCs decreased H9c2 myocardial cell injury by reducing inflammation factor expression during hypoxia induction. The miR-126-enriched exosomes also decreased the expression of fibrosis-related proteins of H9c2 cells under hypoxic conditions. Matrigel® and Transwell® assays showed that miR-126-enriched exosomes significantly promoted microvascular generation and migration, respectively. In vivo studies confirmed that exosomes derived from ADSCs significantly decreased the myocardial injury area of infarction, especially after miR-126-enriched exosome treatment. Cardiac fibrosis and inflammatory cytokine expression were also decreased after treatment with miR-126-enriched exosomes. However, blood vessel formation was promoted in the infarction region of AMI rats. Conclusions: The results suggested that the expression of miR-126-enhanced ADSC-derived exosomes prevented myocardial damage by protecting myocardial cells from apoptosis, inflammation, fibrosis, and increased angiogenesis.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000485949</identifier><identifier>PMID: 29241208</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Acute myocardial ischaemia ; Adipose Tissue - cytology ; Adipose tissues ; ADSCs ; Angiogenesis ; Animals ; Apoptosis ; Cardiomyopathy ; Care and treatment ; Cell Line ; Cell organelles ; Cells, Cultured ; Cellular therapy ; Complications and side effects ; Development and progression ; Exosomes ; Exosomes - genetics ; Gene expression ; Gene Expression Regulation ; Genetic aspects ; Genetic Therapy ; Health aspects ; Heart attack ; Heart attacks ; Heart diseases ; Immunoglobulins ; Inflammation ; Kinases ; Laboratory animals ; Male ; Methods ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MiR-126 ; Myocardial Infarction - genetics ; Myocardial Infarction - pathology ; Myocardial Infarction - therapy ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Neovascularization, Physiologic ; Original Paper ; Physiological aspects ; Rats ; Rats, Sprague-Dawley ; Risk factors ; Rodents ; Stem cells ; Stem Cells - cytology ; Stem Cells - metabolism ; Transplants & implants ; Up-Regulation</subject><ispartof>Cellular Physiology and Biochemistry, 2017-01, Vol.44 (6), p.2105-2116</ispartof><rights>2017 The Author(s). Published by S. Karger AG, Basel</rights><rights>2017 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2018 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c596t-3f6cd7d0c311f10553ff322908ec424c2ed4180cdf0fc9bcab7c3122b94b0e523</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29241208$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Qiancheng</creatorcontrib><creatorcontrib>Guo, Dongfeng</creatorcontrib><creatorcontrib>Liu, Guorong</creatorcontrib><creatorcontrib>Chen, Guo</creatorcontrib><creatorcontrib>Hang, Min</creatorcontrib><creatorcontrib>Jin, Mingming</creatorcontrib><title>Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Recent studies have indicated that exosomes play an important role in adipose-derived stem cell (ADSC) transplant-mediated ischaemic heart disease therapy. However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-126 have a more protective effect on acute myocardial infarction (AMI). Methods: Exosomes were characterized by transmission electron microscopy, and the exosome particles were further examined using nanoparticle tracking analyses. A rat model of myocardial infarction and in vitro model of hypoxia-induced H9c2 myocardial cell injury were established to study the protective mechanism of exosomes from miR-126-overexpressing ADSCs. Results: The in vitro results showed that exosomes derived from miR-126-overexpressing ADSCs decreased H9c2 myocardial cell injury by reducing inflammation factor expression during hypoxia induction. The miR-126-enriched exosomes also decreased the expression of fibrosis-related proteins of H9c2 cells under hypoxic conditions. Matrigel® and Transwell® assays showed that miR-126-enriched exosomes significantly promoted microvascular generation and migration, respectively. In vivo studies confirmed that exosomes derived from ADSCs significantly decreased the myocardial injury area of infarction, especially after miR-126-enriched exosome treatment. Cardiac fibrosis and inflammatory cytokine expression were also decreased after treatment with miR-126-enriched exosomes. However, blood vessel formation was promoted in the infarction region of AMI rats. Conclusions: The results suggested that the expression of miR-126-enhanced ADSC-derived exosomes prevented myocardial damage by protecting myocardial cells from apoptosis, inflammation, fibrosis, and increased angiogenesis.</description><subject>Acute myocardial ischaemia</subject><subject>Adipose Tissue - cytology</subject><subject>Adipose tissues</subject><subject>ADSCs</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cardiomyopathy</subject><subject>Care and treatment</subject><subject>Cell Line</subject><subject>Cell organelles</subject><subject>Cells, Cultured</subject><subject>Cellular therapy</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Exosomes</subject><subject>Exosomes - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Genetic Therapy</subject><subject>Health aspects</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Immunoglobulins</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Methods</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MiR-126</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - therapy</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Neovascularization, Physiologic</subject><subject>Original Paper</subject><subject>Physiological aspects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Transplants & implants</subject><subject>Up-Regulation</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkUFv1DAQhSMEoqVw4I5QJC5wSLEdO7aPy6qFlVoVVeVsOfZ46yWJt3ZSdf993WZZJIR8sD365s2bmaJ4j9Epxkx-RQhRwSSVL4pjTAmuJOfiZX4jzCohBT8q3qS0QfnLJXldHBFJKCZIHBf-7CGk0EMqXQx9eemvK0ya6uoeIjxsI6Tkh3W5sMmkchGhvLmFqLcwjd6UfiivofNw_4yYaYTycheMjtbrrlwlc6uhz9xq2Exx97Z45XSX4N3-Pil-nZ_dLH9UF1ffV8vFRWWYbMaqdo2x3CJTY-wwYqx2riZEIgGGEmoIWIoFMtYhZ2RrdMszSkgraYuAkfqkWM26NuiN2kbf67hTQXv1HAhxrXTM9jtQAllHMMv6tKFtY9pasqxCGws1q7HIWp9nrW0MdxOkUfU-Geg6PUCYksJ50FzUVMqMfvoH3YQpDrlTRTDmmHLGeKZOZ2qtc30_uDBGbfKxT5MKAzif44um5rkTjGhO-DInmBhSiuAOHWGknpavDsvP7Me9hantwR7IP9v-6_G3jmuIB2D589ssobbWZerDf6l9lUfPwrvq</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Luo, Qiancheng</creator><creator>Guo, Dongfeng</creator><creator>Liu, Guorong</creator><creator>Chen, Guo</creator><creator>Hang, Min</creator><creator>Jin, Mingming</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>IAO</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><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20170101</creationdate><title>Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury</title><author>Luo, Qiancheng ; Guo, Dongfeng ; Liu, Guorong ; Chen, Guo ; Hang, Min ; Jin, Mingming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c596t-3f6cd7d0c311f10553ff322908ec424c2ed4180cdf0fc9bcab7c3122b94b0e523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acute myocardial ischaemia</topic><topic>Adipose Tissue - cytology</topic><topic>Adipose tissues</topic><topic>ADSCs</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cardiomyopathy</topic><topic>Care and treatment</topic><topic>Cell Line</topic><topic>Cell organelles</topic><topic>Cells, Cultured</topic><topic>Cellular therapy</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>Exosomes</topic><topic>Exosomes - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genetic aspects</topic><topic>Genetic Therapy</topic><topic>Health aspects</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Immunoglobulins</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Methods</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MiR-126</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - therapy</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Neovascularization, Physiologic</topic><topic>Original Paper</topic><topic>Physiological aspects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>Stem cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>Transplants & implants</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Qiancheng</creatorcontrib><creatorcontrib>Guo, Dongfeng</creatorcontrib><creatorcontrib>Liu, Guorong</creatorcontrib><creatorcontrib>Chen, Guo</creatorcontrib><creatorcontrib>Hang, Min</creatorcontrib><creatorcontrib>Jin, Mingming</creatorcontrib><collection>Karger 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>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & 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 & Medical Complete (Alumni)</collection><collection>Health & 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><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Qiancheng</au><au>Guo, Dongfeng</au><au>Liu, Guorong</au><au>Chen, Guo</au><au>Hang, Min</au><au>Jin, Mingming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>44</volume><issue>6</issue><spage>2105</spage><epage>2116</epage><pages>2105-2116</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Recent studies have indicated that exosomes play an important role in adipose-derived stem cell (ADSC) transplant-mediated ischaemic heart disease therapy. However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-126 have a more protective effect on acute myocardial infarction (AMI). Methods: Exosomes were characterized by transmission electron microscopy, and the exosome particles were further examined using nanoparticle tracking analyses. A rat model of myocardial infarction and in vitro model of hypoxia-induced H9c2 myocardial cell injury were established to study the protective mechanism of exosomes from miR-126-overexpressing ADSCs. Results: The in vitro results showed that exosomes derived from miR-126-overexpressing ADSCs decreased H9c2 myocardial cell injury by reducing inflammation factor expression during hypoxia induction. The miR-126-enriched exosomes also decreased the expression of fibrosis-related proteins of H9c2 cells under hypoxic conditions. Matrigel® and Transwell® assays showed that miR-126-enriched exosomes significantly promoted microvascular generation and migration, respectively. In vivo studies confirmed that exosomes derived from ADSCs significantly decreased the myocardial injury area of infarction, especially after miR-126-enriched exosome treatment. Cardiac fibrosis and inflammatory cytokine expression were also decreased after treatment with miR-126-enriched exosomes. However, blood vessel formation was promoted in the infarction region of AMI rats. Conclusions: The results suggested that the expression of miR-126-enhanced ADSC-derived exosomes prevented myocardial damage by protecting myocardial cells from apoptosis, inflammation, fibrosis, and increased angiogenesis.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29241208</pmid><doi>10.1159/000485949</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute myocardial ischaemia Adipose Tissue - cytology Adipose tissues ADSCs Angiogenesis Animals Apoptosis Cardiomyopathy Care and treatment Cell Line Cell organelles Cells, Cultured Cellular therapy Complications and side effects Development and progression Exosomes Exosomes - genetics Gene expression Gene Expression Regulation Genetic aspects Genetic Therapy Health aspects Heart attack Heart attacks Heart diseases Immunoglobulins Inflammation Kinases Laboratory animals Male Methods MicroRNA MicroRNAs MicroRNAs - genetics MiR-126 Myocardial Infarction - genetics Myocardial Infarction - pathology Myocardial Infarction - therapy Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Neovascularization, Physiologic Original Paper Physiological aspects Rats Rats, Sprague-Dawley Risk factors Rodents Stem cells Stem Cells - cytology Stem Cells - metabolism Transplants & implants Up-Regulation |
| title | Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury |
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