Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice
Abstract Aims The effectiveness of cell-based treatments for regenerative myocardial therapy is limited by low rates of cell engraftment. Y-27632 inhibits Rho-associated protein kinase (ROCK), which regulates the cytoskeletal changes associated with cell adhesion, and has been used to protect cultu...
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| Veröffentlicht in: | Cardiovascular research 2019-02, Vol.115 (2), p.343-356 |
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| creator | Zhao, Meng Fan, Chengming Ernst, Patrick J Tang, Yawen Zhu, Hanxi Mattapally, Saidulu Oduk, Yasin Borovjagin, Anton V Zhou, Lufang Zhang, Jianyi Zhu, Wuqiang |
| description | Abstract
Aims
The effectiveness of cell-based treatments for regenerative myocardial therapy is limited by low rates of cell engraftment. Y-27632 inhibits Rho-associated protein kinase (ROCK), which regulates the cytoskeletal changes associated with cell adhesion, and has been used to protect cultured cells during their passaging. Here, we investigated whether preconditioning of cardiomyocytes, derived from human-induced pluripotent stem cells (hiPSC-CM), with Y-27632 improves their survival and engraftment in a murine model of acute myocardial infarction (MI).
Methods and results
After MI induction, mice were subjected to intramyocardial injections of phosphate-buffered saline, hiPSC-CM cultured under standard conditions (hiPSC-CM–RI), or Y-27632-preconditioned hiPSC-CM (hiPSC-CM+RI). The resulting engraftment rate calculated 4 weeks after implantation was significantly higher and the abundance of apoptotic transplanted cells was significantly lower in hiPSC-CM+RI recipients than in hiPSC-CM–RI animals. In cultured hiPSC-CM, Y-27632-preconditioning reversibly reduced contractile activity and the expression of troponin genes, while increasing their attachment to an underlying mouse cardiomyocyte (HL1) monolayer. Y-27632 preconditioning also increased the expression of N-cadherin and integrin ß1, the two cell junction proteins. hiPSC-CM+RI were also larger in cell area with greater cytoskeletal alignment and a more rod-like shape than hiPSC-CM–RI, both after transplantation (in vivo) and in culture. The effects of Y-27632 preconditioning on contractile activity and morphology of hiPSC-CMs in culture, as well as on their engraftment rate and apoptotic death in MI mouse grafts, could be recapitulated by hiPSC-CM treatment with the L-type calcium-channel blocker verapamil.
Conclusion
Preconditioning with the ROCK inhibitor Y-27632 increased the engraftment of transplanted hiPSC-CM in a murine MI model, while reversibly impairing hiPSC-CM contractility and promoting adhesion. |
| doi_str_mv | 10.1093/cvr/cvy207 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6341224</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/cvr/cvy207</oup_id><sourcerecordid>2088753540</sourcerecordid><originalsourceid>FETCH-LOGICAL-c408t-f24ee1f3d981501e5f454b7ab3b3ba325c7f2e9e51d5ec588951a64eb9d002103</originalsourceid><addsrcrecordid>eNp9kU1LHTEUhkOp6K266Q8o2RSkMJrP-dgUitgqCG7swlXITc54U2aSaZK5cP9Df7SZXpV2IyEkJ-_Lc054EfpIyTklHb8w21j2jpHmHVrRRsqKMyHfoxUhpK1qXvMj9CGlX6WUshGH6IgTShre0RX681CxpuYMTxFM8NZlF7zzjxj8RnsDCeeofZoG7bNeNBx6vJlH7Svn7WzA4mmYo5tCBp9xyjBiA8NQWYhuW1Sjo3Vh3AWzy4XmPF7uy6MeStXraP5iR2fgBB30ekhw-nweo5_fr-4vr6vbux83l99uKyNIm6ueCQDac9u1VBIKshdSrBu95mVpzqRpegYdSGolGNm2naS6FrDuLCGMEn6Mvu6507wewZoyedSDmqIbddypoJ36X_Fuox7DVtVcUMZEAZw9A2L4PUPKanRp-bb2EOakGGnbRnIpll5f9lYTQ0oR-tc2lKglPlXiU_v4ivnTv4O9Wl_yKobPe0OYp7dAT49yqFk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2088753540</pqid></control><display><type>article</type><title>Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Zhao, Meng ; Fan, Chengming ; Ernst, Patrick J ; Tang, Yawen ; Zhu, Hanxi ; Mattapally, Saidulu ; Oduk, Yasin ; Borovjagin, Anton V ; Zhou, Lufang ; Zhang, Jianyi ; Zhu, Wuqiang</creator><creatorcontrib>Zhao, Meng ; Fan, Chengming ; Ernst, Patrick J ; Tang, Yawen ; Zhu, Hanxi ; Mattapally, Saidulu ; Oduk, Yasin ; Borovjagin, Anton V ; Zhou, Lufang ; Zhang, Jianyi ; Zhu, Wuqiang</creatorcontrib><description>Abstract
Aims
The effectiveness of cell-based treatments for regenerative myocardial therapy is limited by low rates of cell engraftment. Y-27632 inhibits Rho-associated protein kinase (ROCK), which regulates the cytoskeletal changes associated with cell adhesion, and has been used to protect cultured cells during their passaging. Here, we investigated whether preconditioning of cardiomyocytes, derived from human-induced pluripotent stem cells (hiPSC-CM), with Y-27632 improves their survival and engraftment in a murine model of acute myocardial infarction (MI).
Methods and results
After MI induction, mice were subjected to intramyocardial injections of phosphate-buffered saline, hiPSC-CM cultured under standard conditions (hiPSC-CM–RI), or Y-27632-preconditioned hiPSC-CM (hiPSC-CM+RI). The resulting engraftment rate calculated 4 weeks after implantation was significantly higher and the abundance of apoptotic transplanted cells was significantly lower in hiPSC-CM+RI recipients than in hiPSC-CM–RI animals. In cultured hiPSC-CM, Y-27632-preconditioning reversibly reduced contractile activity and the expression of troponin genes, while increasing their attachment to an underlying mouse cardiomyocyte (HL1) monolayer. Y-27632 preconditioning also increased the expression of N-cadherin and integrin ß1, the two cell junction proteins. hiPSC-CM+RI were also larger in cell area with greater cytoskeletal alignment and a more rod-like shape than hiPSC-CM–RI, both after transplantation (in vivo) and in culture. The effects of Y-27632 preconditioning on contractile activity and morphology of hiPSC-CMs in culture, as well as on their engraftment rate and apoptotic death in MI mouse grafts, could be recapitulated by hiPSC-CM treatment with the L-type calcium-channel blocker verapamil.
Conclusion
Preconditioning with the ROCK inhibitor Y-27632 increased the engraftment of transplanted hiPSC-CM in a murine MI model, while reversibly impairing hiPSC-CM contractility and promoting adhesion.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1093/cvr/cvy207</identifier><identifier>PMID: 30107391</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Amides - pharmacology ; Animals ; Apoptosis - drug effects ; Cell Adhesion - drug effects ; Cell Differentiation ; Cell Survival - drug effects ; Cells, Cultured ; Disease Models, Animal ; Graft Survival - drug effects ; Humans ; Induced Pluripotent Stem Cells - drug effects ; Induced Pluripotent Stem Cells - enzymology ; Induced Pluripotent Stem Cells - transplantation ; Mice, Inbred NOD ; Mice, SCID ; Myocardial Contraction - drug effects ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocardial Infarction - surgery ; Myocardium - metabolism ; Myocardium - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - enzymology ; Myocytes, Cardiac - transplantation ; Original ; Phenotype ; Protein Kinase Inhibitors - pharmacology ; Pyridines - pharmacology ; Recovery of Function ; rho-Associated Kinases - antagonists & inhibitors ; rho-Associated Kinases - metabolism ; Time Factors</subject><ispartof>Cardiovascular research, 2019-02, Vol.115 (2), p.343-356</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-f24ee1f3d981501e5f454b7ab3b3ba325c7f2e9e51d5ec588951a64eb9d002103</citedby><cites>FETCH-LOGICAL-c408t-f24ee1f3d981501e5f454b7ab3b3ba325c7f2e9e51d5ec588951a64eb9d002103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30107391$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Meng</creatorcontrib><creatorcontrib>Fan, Chengming</creatorcontrib><creatorcontrib>Ernst, Patrick J</creatorcontrib><creatorcontrib>Tang, Yawen</creatorcontrib><creatorcontrib>Zhu, Hanxi</creatorcontrib><creatorcontrib>Mattapally, Saidulu</creatorcontrib><creatorcontrib>Oduk, Yasin</creatorcontrib><creatorcontrib>Borovjagin, Anton V</creatorcontrib><creatorcontrib>Zhou, Lufang</creatorcontrib><creatorcontrib>Zhang, Jianyi</creatorcontrib><creatorcontrib>Zhu, Wuqiang</creatorcontrib><title>Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>Abstract
Aims
The effectiveness of cell-based treatments for regenerative myocardial therapy is limited by low rates of cell engraftment. Y-27632 inhibits Rho-associated protein kinase (ROCK), which regulates the cytoskeletal changes associated with cell adhesion, and has been used to protect cultured cells during their passaging. Here, we investigated whether preconditioning of cardiomyocytes, derived from human-induced pluripotent stem cells (hiPSC-CM), with Y-27632 improves their survival and engraftment in a murine model of acute myocardial infarction (MI).
Methods and results
After MI induction, mice were subjected to intramyocardial injections of phosphate-buffered saline, hiPSC-CM cultured under standard conditions (hiPSC-CM–RI), or Y-27632-preconditioned hiPSC-CM (hiPSC-CM+RI). The resulting engraftment rate calculated 4 weeks after implantation was significantly higher and the abundance of apoptotic transplanted cells was significantly lower in hiPSC-CM+RI recipients than in hiPSC-CM–RI animals. In cultured hiPSC-CM, Y-27632-preconditioning reversibly reduced contractile activity and the expression of troponin genes, while increasing their attachment to an underlying mouse cardiomyocyte (HL1) monolayer. Y-27632 preconditioning also increased the expression of N-cadherin and integrin ß1, the two cell junction proteins. hiPSC-CM+RI were also larger in cell area with greater cytoskeletal alignment and a more rod-like shape than hiPSC-CM–RI, both after transplantation (in vivo) and in culture. The effects of Y-27632 preconditioning on contractile activity and morphology of hiPSC-CMs in culture, as well as on their engraftment rate and apoptotic death in MI mouse grafts, could be recapitulated by hiPSC-CM treatment with the L-type calcium-channel blocker verapamil.
Conclusion
Preconditioning with the ROCK inhibitor Y-27632 increased the engraftment of transplanted hiPSC-CM in a murine MI model, while reversibly impairing hiPSC-CM contractility and promoting adhesion.</description><subject>Amides - pharmacology</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Differentiation</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Graft Survival - drug effects</subject><subject>Humans</subject><subject>Induced Pluripotent Stem Cells - drug effects</subject><subject>Induced Pluripotent Stem Cells - enzymology</subject><subject>Induced Pluripotent Stem Cells - transplantation</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Infarction - surgery</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Myocytes, Cardiac - transplantation</subject><subject>Original</subject><subject>Phenotype</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Pyridines - pharmacology</subject><subject>Recovery of Function</subject><subject>rho-Associated Kinases - antagonists & inhibitors</subject><subject>rho-Associated Kinases - metabolism</subject><subject>Time Factors</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1LHTEUhkOp6K266Q8o2RSkMJrP-dgUitgqCG7swlXITc54U2aSaZK5cP9Df7SZXpV2IyEkJ-_Lc054EfpIyTklHb8w21j2jpHmHVrRRsqKMyHfoxUhpK1qXvMj9CGlX6WUshGH6IgTShre0RX681CxpuYMTxFM8NZlF7zzjxj8RnsDCeeofZoG7bNeNBx6vJlH7Svn7WzA4mmYo5tCBp9xyjBiA8NQWYhuW1Sjo3Vh3AWzy4XmPF7uy6MeStXraP5iR2fgBB30ekhw-nweo5_fr-4vr6vbux83l99uKyNIm6ueCQDac9u1VBIKshdSrBu95mVpzqRpegYdSGolGNm2naS6FrDuLCGMEn6Mvu6507wewZoyedSDmqIbddypoJ36X_Fuox7DVtVcUMZEAZw9A2L4PUPKanRp-bb2EOakGGnbRnIpll5f9lYTQ0oR-tc2lKglPlXiU_v4ivnTv4O9Wl_yKobPe0OYp7dAT49yqFk</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Zhao, Meng</creator><creator>Fan, Chengming</creator><creator>Ernst, Patrick J</creator><creator>Tang, Yawen</creator><creator>Zhu, Hanxi</creator><creator>Mattapally, Saidulu</creator><creator>Oduk, Yasin</creator><creator>Borovjagin, Anton V</creator><creator>Zhou, Lufang</creator><creator>Zhang, Jianyi</creator><creator>Zhu, Wuqiang</creator><general>Oxford University Press</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190201</creationdate><title>Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice</title><author>Zhao, Meng ; Fan, Chengming ; Ernst, Patrick J ; Tang, Yawen ; Zhu, Hanxi ; Mattapally, Saidulu ; Oduk, Yasin ; Borovjagin, Anton V ; Zhou, Lufang ; Zhang, Jianyi ; Zhu, Wuqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-f24ee1f3d981501e5f454b7ab3b3ba325c7f2e9e51d5ec588951a64eb9d002103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Amides - pharmacology</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Differentiation</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Graft Survival - drug effects</topic><topic>Humans</topic><topic>Induced Pluripotent Stem Cells - drug effects</topic><topic>Induced Pluripotent Stem Cells - enzymology</topic><topic>Induced Pluripotent Stem Cells - transplantation</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Infarction - surgery</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Myocytes, Cardiac - transplantation</topic><topic>Original</topic><topic>Phenotype</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Pyridines - pharmacology</topic><topic>Recovery of Function</topic><topic>rho-Associated Kinases - antagonists & inhibitors</topic><topic>rho-Associated Kinases - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Meng</creatorcontrib><creatorcontrib>Fan, Chengming</creatorcontrib><creatorcontrib>Ernst, Patrick J</creatorcontrib><creatorcontrib>Tang, Yawen</creatorcontrib><creatorcontrib>Zhu, Hanxi</creatorcontrib><creatorcontrib>Mattapally, Saidulu</creatorcontrib><creatorcontrib>Oduk, Yasin</creatorcontrib><creatorcontrib>Borovjagin, Anton V</creatorcontrib><creatorcontrib>Zhou, Lufang</creatorcontrib><creatorcontrib>Zhang, Jianyi</creatorcontrib><creatorcontrib>Zhu, Wuqiang</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Meng</au><au>Fan, Chengming</au><au>Ernst, Patrick J</au><au>Tang, Yawen</au><au>Zhu, Hanxi</au><au>Mattapally, Saidulu</au><au>Oduk, Yasin</au><au>Borovjagin, Anton V</au><au>Zhou, Lufang</au><au>Zhang, Jianyi</au><au>Zhu, Wuqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>115</volume><issue>2</issue><spage>343</spage><epage>356</epage><pages>343-356</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><abstract>Abstract
Aims
The effectiveness of cell-based treatments for regenerative myocardial therapy is limited by low rates of cell engraftment. Y-27632 inhibits Rho-associated protein kinase (ROCK), which regulates the cytoskeletal changes associated with cell adhesion, and has been used to protect cultured cells during their passaging. Here, we investigated whether preconditioning of cardiomyocytes, derived from human-induced pluripotent stem cells (hiPSC-CM), with Y-27632 improves their survival and engraftment in a murine model of acute myocardial infarction (MI).
Methods and results
After MI induction, mice were subjected to intramyocardial injections of phosphate-buffered saline, hiPSC-CM cultured under standard conditions (hiPSC-CM–RI), or Y-27632-preconditioned hiPSC-CM (hiPSC-CM+RI). The resulting engraftment rate calculated 4 weeks after implantation was significantly higher and the abundance of apoptotic transplanted cells was significantly lower in hiPSC-CM+RI recipients than in hiPSC-CM–RI animals. In cultured hiPSC-CM, Y-27632-preconditioning reversibly reduced contractile activity and the expression of troponin genes, while increasing their attachment to an underlying mouse cardiomyocyte (HL1) monolayer. Y-27632 preconditioning also increased the expression of N-cadherin and integrin ß1, the two cell junction proteins. hiPSC-CM+RI were also larger in cell area with greater cytoskeletal alignment and a more rod-like shape than hiPSC-CM–RI, both after transplantation (in vivo) and in culture. The effects of Y-27632 preconditioning on contractile activity and morphology of hiPSC-CMs in culture, as well as on their engraftment rate and apoptotic death in MI mouse grafts, could be recapitulated by hiPSC-CM treatment with the L-type calcium-channel blocker verapamil.
Conclusion
Preconditioning with the ROCK inhibitor Y-27632 increased the engraftment of transplanted hiPSC-CM in a murine MI model, while reversibly impairing hiPSC-CM contractility and promoting adhesion.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>30107391</pmid><doi>10.1093/cvr/cvy207</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cardiovascular research, 2019-02, Vol.115 (2), p.343-356 |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Amides - pharmacology Animals Apoptosis - drug effects Cell Adhesion - drug effects Cell Differentiation Cell Survival - drug effects Cells, Cultured Disease Models, Animal Graft Survival - drug effects Humans Induced Pluripotent Stem Cells - drug effects Induced Pluripotent Stem Cells - enzymology Induced Pluripotent Stem Cells - transplantation Mice, Inbred NOD Mice, SCID Myocardial Contraction - drug effects Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocardial Infarction - surgery Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - enzymology Myocytes, Cardiac - transplantation Original Phenotype Protein Kinase Inhibitors - pharmacology Pyridines - pharmacology Recovery of Function rho-Associated Kinases - antagonists & inhibitors rho-Associated Kinases - metabolism Time Factors |
| title | Y-27632 preconditioning enhances transplantation of human-induced pluripotent stem cell-derived cardiomyocytes in myocardial infarction mice |
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