Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair
Extracellular vesicles (EVs) from stem cells have shown significant therapeutic potential to repair injured cardiac tissues and regulate pathological fibrosis. However, scalable generation of stem cells and derived EVs for clinical utility remains a huge technical challenge. Here, we report a rapid...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2022-11, Vol.23 (22), p.14334 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 22 |
| container_start_page | 14334 |
| container_title | International journal of molecular sciences |
| container_volume | 23 |
| creator | Lozano, Jonathan Rai, Alin Lees, Jarmon G Fang, Haoyun Claridge, Bethany Lim, Shiang Y Greening, David W |
| description | Extracellular vesicles (EVs) from stem cells have shown significant therapeutic potential to repair injured cardiac tissues and regulate pathological fibrosis. However, scalable generation of stem cells and derived EVs for clinical utility remains a huge technical challenge. Here, we report a rapid size-based extrusion strategy to generate EV-like membranous nanovesicles (NVs) from easily sourced human iPSCs in large quantities (yield 900× natural EVs). NVs isolated using density-gradient separation (buoyant density 1.13 g/mL) are spherical in shape and morphologically intact and readily internalised by human cardiomyocytes, primary cardiac fibroblasts, and endothelial cells. NVs captured the dynamic proteome of parental cells and include pluripotency markers (LIN28A, OCT4) and regulators of cardiac repair processes, including tissue repair (GJA1, HSP20/27/70, HMGB1), wound healing (FLNA, MYH9, ACTC1, ILK), stress response/translation initiation (eIF2S1/S2/S3/B4), hypoxia response (HMOX2, HSP90, GNB1), and extracellular matrix organization (ITGA6, MFGE8, ITGB1). Functionally, NVs significantly promoted tubule formation of endothelial cells (angiogenesis) (p < 0.05) and survival of cardiomyocytes exposed to low oxygen conditions (hypoxia) (p < 0.0001), as well as attenuated TGF-β mediated activation of cardiac fibroblasts (p < 0.0001). Quantitative proteome profiling of target cell proteome following NV treatments revealed upregulation of angiogenic proteins (MFGE8, MYH10, VDAC2) in endothelial cells and pro-survival proteins (CNN2, THBS1, IGF2R) in cardiomyocytes. In contrast, NVs attenuated TGF-β-driven extracellular matrix remodelling capacity in cardiac fibroblasts (ACTN1, COL1A1/2/4A2/12A1, ITGA1/11, THBS1). This study presents a scalable approach to generating functional NVs for cardiac repair. |
| doi_str_mv | 10.3390/ijms232214334 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9696585</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2739445146</sourcerecordid><originalsourceid>FETCH-LOGICAL-c415t-3deccd412ecf20b78eae6bc8442ea72095461c5b9d23ea39af773def4ddbfe773</originalsourceid><addsrcrecordid>eNpdkc1LHEEQxZtgcNV4zFUavHgZ01_zdRFkMbogSYjJuVPTXaO9zHSv3TNC_vu0uMqaUz2oXz3q8Qj5zNm5lC374tZjElIIrqRUH8gBV0IUjFX13o5ekMOU1oxlsGz3yUJWSrKGiwPy587AAN2A9Bo9Rphc8DT09Bv48ITJmQET7WMY6c08gi9W3s4GLf0xzNFtwoR-oncTjnSJw5DJEOkSonVg6E_cgIufyMcehoTH23lEfn-9-rW8KW6_X6-Wl7eFUbycCmnRGKu4QNML1tUNAladaZQSCLVgbakqbsqutUIiyBb6us43vbK26zHrI3Lx4ruZuxGtyY9FGPQmuhHiXx3A6fcb7x70fXjSbdVWZVNmg7OtQQyPM6ZJjy6ZnAo8hjlpUStWsqYSTUZP_0PXYY4-x8uUbJUquaoyVbxQJoaUIvZvz3Cmn7vT77rL_Mlugjf6tSz5D5dnlyY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2739445146</pqid></control><display><type>article</type><title>Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Lozano, Jonathan ; Rai, Alin ; Lees, Jarmon G ; Fang, Haoyun ; Claridge, Bethany ; Lim, Shiang Y ; Greening, David W</creator><creatorcontrib>Lozano, Jonathan ; Rai, Alin ; Lees, Jarmon G ; Fang, Haoyun ; Claridge, Bethany ; Lim, Shiang Y ; Greening, David W</creatorcontrib><description>Extracellular vesicles (EVs) from stem cells have shown significant therapeutic potential to repair injured cardiac tissues and regulate pathological fibrosis. However, scalable generation of stem cells and derived EVs for clinical utility remains a huge technical challenge. Here, we report a rapid size-based extrusion strategy to generate EV-like membranous nanovesicles (NVs) from easily sourced human iPSCs in large quantities (yield 900× natural EVs). NVs isolated using density-gradient separation (buoyant density 1.13 g/mL) are spherical in shape and morphologically intact and readily internalised by human cardiomyocytes, primary cardiac fibroblasts, and endothelial cells. NVs captured the dynamic proteome of parental cells and include pluripotency markers (LIN28A, OCT4) and regulators of cardiac repair processes, including tissue repair (GJA1, HSP20/27/70, HMGB1), wound healing (FLNA, MYH9, ACTC1, ILK), stress response/translation initiation (eIF2S1/S2/S3/B4), hypoxia response (HMOX2, HSP90, GNB1), and extracellular matrix organization (ITGA6, MFGE8, ITGB1). Functionally, NVs significantly promoted tubule formation of endothelial cells (angiogenesis) (p < 0.05) and survival of cardiomyocytes exposed to low oxygen conditions (hypoxia) (p < 0.0001), as well as attenuated TGF-β mediated activation of cardiac fibroblasts (p < 0.0001). Quantitative proteome profiling of target cell proteome following NV treatments revealed upregulation of angiogenic proteins (MFGE8, MYH10, VDAC2) in endothelial cells and pro-survival proteins (CNN2, THBS1, IGF2R) in cardiomyocytes. In contrast, NVs attenuated TGF-β-driven extracellular matrix remodelling capacity in cardiac fibroblasts (ACTN1, COL1A1/2/4A2/12A1, ITGA1/11, THBS1). This study presents a scalable approach to generating functional NVs for cardiac repair.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms232214334</identifier><identifier>PMID: 36430812</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Angiogenesis ; Cardiomyocytes ; Cluster analysis ; Collagen (type I) ; Connexin 43 ; Endothelial cells ; Endothelial Cells - metabolism ; Extracellular matrix ; Extracellular vesicles ; Fibroblasts ; Fibrosis ; Gap junctions ; Heart ; HMGB1 protein ; Hsp90 protein ; Human influences ; Humans ; Hypoxia ; Hypoxia - metabolism ; ILK protein ; Induced Pluripotent Stem Cells ; Insulin-like growth factor II receptors ; Ischemia ; Mass spectrometry ; Microscopy ; Morphology ; Nanoparticles ; Oct-4 protein ; Ontology ; Pluripotency ; Protein expression ; Proteins ; Proteome - metabolism ; Proteomes ; Scientific imaging ; Stem cells ; Survival ; Transforming Growth Factor beta - metabolism ; Translation initiation ; Wound healing</subject><ispartof>International journal of molecular sciences, 2022-11, Vol.23 (22), p.14334</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-3deccd412ecf20b78eae6bc8442ea72095461c5b9d23ea39af773def4ddbfe773</citedby><cites>FETCH-LOGICAL-c415t-3deccd412ecf20b78eae6bc8442ea72095461c5b9d23ea39af773def4ddbfe773</cites><orcidid>0000-0002-0442-3655 ; 0000-0002-9259-8657 ; 0000-0002-5361-8002 ; 0000-0001-7516-485X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696585/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696585/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36430812$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lozano, Jonathan</creatorcontrib><creatorcontrib>Rai, Alin</creatorcontrib><creatorcontrib>Lees, Jarmon G</creatorcontrib><creatorcontrib>Fang, Haoyun</creatorcontrib><creatorcontrib>Claridge, Bethany</creatorcontrib><creatorcontrib>Lim, Shiang Y</creatorcontrib><creatorcontrib>Greening, David W</creatorcontrib><title>Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Extracellular vesicles (EVs) from stem cells have shown significant therapeutic potential to repair injured cardiac tissues and regulate pathological fibrosis. However, scalable generation of stem cells and derived EVs for clinical utility remains a huge technical challenge. Here, we report a rapid size-based extrusion strategy to generate EV-like membranous nanovesicles (NVs) from easily sourced human iPSCs in large quantities (yield 900× natural EVs). NVs isolated using density-gradient separation (buoyant density 1.13 g/mL) are spherical in shape and morphologically intact and readily internalised by human cardiomyocytes, primary cardiac fibroblasts, and endothelial cells. NVs captured the dynamic proteome of parental cells and include pluripotency markers (LIN28A, OCT4) and regulators of cardiac repair processes, including tissue repair (GJA1, HSP20/27/70, HMGB1), wound healing (FLNA, MYH9, ACTC1, ILK), stress response/translation initiation (eIF2S1/S2/S3/B4), hypoxia response (HMOX2, HSP90, GNB1), and extracellular matrix organization (ITGA6, MFGE8, ITGB1). Functionally, NVs significantly promoted tubule formation of endothelial cells (angiogenesis) (p < 0.05) and survival of cardiomyocytes exposed to low oxygen conditions (hypoxia) (p < 0.0001), as well as attenuated TGF-β mediated activation of cardiac fibroblasts (p < 0.0001). Quantitative proteome profiling of target cell proteome following NV treatments revealed upregulation of angiogenic proteins (MFGE8, MYH10, VDAC2) in endothelial cells and pro-survival proteins (CNN2, THBS1, IGF2R) in cardiomyocytes. In contrast, NVs attenuated TGF-β-driven extracellular matrix remodelling capacity in cardiac fibroblasts (ACTN1, COL1A1/2/4A2/12A1, ITGA1/11, THBS1). This study presents a scalable approach to generating functional NVs for cardiac repair.</description><subject>Angiogenesis</subject><subject>Cardiomyocytes</subject><subject>Cluster analysis</subject><subject>Collagen (type I)</subject><subject>Connexin 43</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Extracellular matrix</subject><subject>Extracellular vesicles</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Gap junctions</subject><subject>Heart</subject><subject>HMGB1 protein</subject><subject>Hsp90 protein</subject><subject>Human influences</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia - metabolism</subject><subject>ILK protein</subject><subject>Induced Pluripotent Stem Cells</subject><subject>Insulin-like growth factor II receptors</subject><subject>Ischemia</subject><subject>Mass spectrometry</subject><subject>Microscopy</subject><subject>Morphology</subject><subject>Nanoparticles</subject><subject>Oct-4 protein</subject><subject>Ontology</subject><subject>Pluripotency</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proteome - metabolism</subject><subject>Proteomes</subject><subject>Scientific imaging</subject><subject>Stem cells</subject><subject>Survival</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Translation initiation</subject><subject>Wound healing</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LHEEQxZtgcNV4zFUavHgZ01_zdRFkMbogSYjJuVPTXaO9zHSv3TNC_vu0uMqaUz2oXz3q8Qj5zNm5lC374tZjElIIrqRUH8gBV0IUjFX13o5ekMOU1oxlsGz3yUJWSrKGiwPy587AAN2A9Bo9Rphc8DT09Bv48ITJmQET7WMY6c08gi9W3s4GLf0xzNFtwoR-oncTjnSJw5DJEOkSonVg6E_cgIufyMcehoTH23lEfn-9-rW8KW6_X6-Wl7eFUbycCmnRGKu4QNML1tUNAladaZQSCLVgbakqbsqutUIiyBb6us43vbK26zHrI3Lx4ruZuxGtyY9FGPQmuhHiXx3A6fcb7x70fXjSbdVWZVNmg7OtQQyPM6ZJjy6ZnAo8hjlpUStWsqYSTUZP_0PXYY4-x8uUbJUquaoyVbxQJoaUIvZvz3Cmn7vT77rL_Mlugjf6tSz5D5dnlyY</recordid><startdate>20221118</startdate><enddate>20221118</enddate><creator>Lozano, Jonathan</creator><creator>Rai, Alin</creator><creator>Lees, Jarmon G</creator><creator>Fang, Haoyun</creator><creator>Claridge, Bethany</creator><creator>Lim, Shiang Y</creator><creator>Greening, David W</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0442-3655</orcidid><orcidid>https://orcid.org/0000-0002-9259-8657</orcidid><orcidid>https://orcid.org/0000-0002-5361-8002</orcidid><orcidid>https://orcid.org/0000-0001-7516-485X</orcidid></search><sort><creationdate>20221118</creationdate><title>Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair</title><author>Lozano, Jonathan ; Rai, Alin ; Lees, Jarmon G ; Fang, Haoyun ; Claridge, Bethany ; Lim, Shiang Y ; Greening, David W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-3deccd412ecf20b78eae6bc8442ea72095461c5b9d23ea39af773def4ddbfe773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiogenesis</topic><topic>Cardiomyocytes</topic><topic>Cluster analysis</topic><topic>Collagen (type I)</topic><topic>Connexin 43</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Extracellular matrix</topic><topic>Extracellular vesicles</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Gap junctions</topic><topic>Heart</topic><topic>HMGB1 protein</topic><topic>Hsp90 protein</topic><topic>Human influences</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia - metabolism</topic><topic>ILK protein</topic><topic>Induced Pluripotent Stem Cells</topic><topic>Insulin-like growth factor II receptors</topic><topic>Ischemia</topic><topic>Mass spectrometry</topic><topic>Microscopy</topic><topic>Morphology</topic><topic>Nanoparticles</topic><topic>Oct-4 protein</topic><topic>Ontology</topic><topic>Pluripotency</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proteome - metabolism</topic><topic>Proteomes</topic><topic>Scientific imaging</topic><topic>Stem cells</topic><topic>Survival</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Translation initiation</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lozano, Jonathan</creatorcontrib><creatorcontrib>Rai, Alin</creatorcontrib><creatorcontrib>Lees, Jarmon G</creatorcontrib><creatorcontrib>Fang, Haoyun</creatorcontrib><creatorcontrib>Claridge, Bethany</creatorcontrib><creatorcontrib>Lim, Shiang Y</creatorcontrib><creatorcontrib>Greening, David W</creatorcontrib><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>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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lozano, Jonathan</au><au>Rai, Alin</au><au>Lees, Jarmon G</au><au>Fang, Haoyun</au><au>Claridge, Bethany</au><au>Lim, Shiang Y</au><au>Greening, David W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-11-18</date><risdate>2022</risdate><volume>23</volume><issue>22</issue><spage>14334</spage><pages>14334-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Extracellular vesicles (EVs) from stem cells have shown significant therapeutic potential to repair injured cardiac tissues and regulate pathological fibrosis. However, scalable generation of stem cells and derived EVs for clinical utility remains a huge technical challenge. Here, we report a rapid size-based extrusion strategy to generate EV-like membranous nanovesicles (NVs) from easily sourced human iPSCs in large quantities (yield 900× natural EVs). NVs isolated using density-gradient separation (buoyant density 1.13 g/mL) are spherical in shape and morphologically intact and readily internalised by human cardiomyocytes, primary cardiac fibroblasts, and endothelial cells. NVs captured the dynamic proteome of parental cells and include pluripotency markers (LIN28A, OCT4) and regulators of cardiac repair processes, including tissue repair (GJA1, HSP20/27/70, HMGB1), wound healing (FLNA, MYH9, ACTC1, ILK), stress response/translation initiation (eIF2S1/S2/S3/B4), hypoxia response (HMOX2, HSP90, GNB1), and extracellular matrix organization (ITGA6, MFGE8, ITGB1). Functionally, NVs significantly promoted tubule formation of endothelial cells (angiogenesis) (p < 0.05) and survival of cardiomyocytes exposed to low oxygen conditions (hypoxia) (p < 0.0001), as well as attenuated TGF-β mediated activation of cardiac fibroblasts (p < 0.0001). Quantitative proteome profiling of target cell proteome following NV treatments revealed upregulation of angiogenic proteins (MFGE8, MYH10, VDAC2) in endothelial cells and pro-survival proteins (CNN2, THBS1, IGF2R) in cardiomyocytes. In contrast, NVs attenuated TGF-β-driven extracellular matrix remodelling capacity in cardiac fibroblasts (ACTN1, COL1A1/2/4A2/12A1, ITGA1/11, THBS1). This study presents a scalable approach to generating functional NVs for cardiac repair.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36430812</pmid><doi>10.3390/ijms232214334</doi><orcidid>https://orcid.org/0000-0002-0442-3655</orcidid><orcidid>https://orcid.org/0000-0002-9259-8657</orcidid><orcidid>https://orcid.org/0000-0002-5361-8002</orcidid><orcidid>https://orcid.org/0000-0001-7516-485X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2022-11, Vol.23 (22), p.14334 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9696585 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Angiogenesis Cardiomyocytes Cluster analysis Collagen (type I) Connexin 43 Endothelial cells Endothelial Cells - metabolism Extracellular matrix Extracellular vesicles Fibroblasts Fibrosis Gap junctions Heart HMGB1 protein Hsp90 protein Human influences Humans Hypoxia Hypoxia - metabolism ILK protein Induced Pluripotent Stem Cells Insulin-like growth factor II receptors Ischemia Mass spectrometry Microscopy Morphology Nanoparticles Oct-4 protein Ontology Pluripotency Protein expression Proteins Proteome - metabolism Proteomes Scientific imaging Stem cells Survival Transforming Growth Factor beta - metabolism Translation initiation Wound healing |
| title | Scalable Generation of Nanovesicles from Human-Induced Pluripotent Stem Cells for Cardiac Repair |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T06%3A02%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Scalable%20Generation%20of%20Nanovesicles%20from%20Human-Induced%20Pluripotent%20Stem%20Cells%20for%20Cardiac%20Repair&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Lozano,%20Jonathan&rft.date=2022-11-18&rft.volume=23&rft.issue=22&rft.spage=14334&rft.pages=14334-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms232214334&rft_dat=%3Cproquest_pubme%3E2739445146%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2739445146&rft_id=info:pmid/36430812&rfr_iscdi=true |