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dc.contributor.authorChoi, Jung-Kyun-
dc.contributor.authorChung, Haeun-
dc.contributor.authorOh, Seung Ja-
dc.contributor.authorKim, Jong-Wan-
dc.contributor.authorKim, Sang-Heon-
dc.date.accessioned2024-01-19T09:02:37Z-
dc.date.available2024-01-19T09:02:37Z-
dc.date.created2023-08-02-
dc.date.issued2023-08-
dc.identifier.issn1742-7061-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/113433-
dc.description.abstractStem cell therapy has emerged as a promising regenerative medicine strategy but is limited by poor cell survival, leading to low therapeutic outcomes. We developed cell spheroid therapeutics to overcome this limitation. We utilized solid-phase FGF2 to form functionally enhanced cell spheroid-adipose derived (FECS-Ad), a type of cell spheroid that preconditions cells with intrinsic hypoxia to increase the survival of transplanted cells. We demonstrated an increase in hypoxia-inducible factor 1-alpha (HIF-1 & alpha;) levels in FECS-Ad, which led to the upregulation of tissue inhibitor of metalloproteinase 1 (TIMP1). TIMP1 enhanced the survival of FECS-Ad, presumably through the CD63/FAK/Akt/Bcl2 anti-apoptotic signaling pathway. Cell viability of transplanted FECS-Ad was reduced by TIMP1 knockdown in an in vitro collagen gel block and a mouse model of critical limb ischemia (CLI). TIMP1 knockdown in FECS-Ad inhibited angiogenesis and muscle regeneration induced by FECS-Ad transplanted into ischemic mouse tissue. Genetic overexpression of TIMP1 in FECS-Ad further promoted the survival and therapeutic efficacy of transplanted FECS-Ad. Collectively, we suggest that TIMP1 acts as a key survival factor to improve the survival of transplanted stem cell spheroids, which provides scientific evidence for enhanced therapeutic efficacy of stem cell spheroids, and FECS-Ad as a potential therapeutic agent to treat CLI.-
dc.languageEnglish-
dc.publisherElsevier BV-
dc.titleFunctionally enhanced cell spheroids for stem cell therapy: Role of TIMP1 in the survival and therapeutic effectiveness of stem cell spheroids-
dc.typeArticle-
dc.identifier.doi10.1016/j.actbio.2023.05.033-
dc.description.journalClass1-
dc.identifier.bibliographicCitationActa Biomaterialia, v.166, pp.454 - 469-
dc.citation.titleActa Biomaterialia-
dc.citation.volume166-
dc.citation.startPage454-
dc.citation.endPage469-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid001031572300001-
dc.identifier.scopusid2-s2.0-85163348050-
dc.relation.journalWebOfScienceCategoryEngineering, Biomedical-
dc.relation.journalWebOfScienceCategoryMaterials Science, Biomaterials-
dc.relation.journalResearchAreaEngineering-
dc.relation.journalResearchAreaMaterials Science-
dc.type.docTypeArticle-
dc.subject.keywordPlusBREAST EPITHELIAL-CELLS-
dc.subject.keywordPlusTISSUE INHIBITOR-
dc.subject.keywordPlusINFARCTED HEART-
dc.subject.keywordPlusGROWTH-FACTOR-
dc.subject.keywordPlusADHESION-
dc.subject.keywordPlusDIFFERENTIATION-
dc.subject.keywordPlusTRANSPLANTATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusDEATH-
dc.subject.keywordPlusMETALLOPROTEINASE-1-
dc.subject.keywordAuthorTissue inhibitor matrix metalloproteinase 1-
dc.subject.keywordAuthorSpheroid-
dc.subject.keywordAuthorCritical limb ischemia-
dc.subject.keywordAuthorStem cell therapy-
dc.subject.keywordAuthorSurvival-
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