File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Bradykinin-pretreated Human cardiac-specific c-kit(+) Cells Enhance Exosomal miR-3059-5p and Promote Angiogenesis Against Hindlimb Ischemia in mice

TitleBradykinin-pretreated Human cardiac-specific c-kit(+) Cells Enhance Exosomal miR-3059-5p and Promote Angiogenesis Against Hindlimb Ischemia in mice
Authors
Keywordsangiogenesis
Bradykinin
cardiac-specific c-kit+ cells
exosome
miR-3059-5p
TNFSF15
Issue Date1-Oct-2023
PublisherSpringer
Citation
Stem Cell Reviews and Reports, 2023, v. 19, n. 7, p. 2481-2496 How to Cite?
Abstract

BackgroundProtection of cardiac function following myocardial infarction was largely enhanced by bradykinin-pretreated cardiac-specific c-kit(+) (BK-c-kit(+)) cells, even without significant engraftment, indicating that paracrine actions of BK-c-kit(+) cells play a pivotal role in angiogenesis. Nevertheless, the active components of the paracrine actions of BK-c-kit(+) cells and the underlying mechanisms remain unknown. This study aimed to define the active components of exosomes from BK-c-kit(+) cells and elucidate their underlying protective mechanisms.MethodsMatrigel tube formation assay, cell cycle, and mobility in human umbilical vein endothelial cells (HUVECs) and hindlimb ischemia (HLI) in mice were applied to determine the angiogenic effect of condition medium (CM) and exosomes. Proteome profiler, microRNA sponge, Due-luciferase assay, microRNA-sequencing, qRT-PCR, and Western blot were used to determine the underlying mechanism of the angiogenic effect of exosomes from BK-c-kit(+).ResultsAs a result, BK-c-kit(+) CM and exosomes promoted tube formation in HUVECs and the repair of HLI in mice. Angiogenesis-related proteomic profiling and microRNA sequencing revealed highly enriched miR-3059-5p as a key angiogenic component of BK-c-kit(+) exosomes. Meanwhile, loss- and gain-of-function experiments revealed that the promotion of angiogenesis by miR-3059-5p was mainly through suppression of TNFSF15-inhibited effects on vascular tube formation, cell proliferation and cell migration. Moreover, enhanced angiogenesis of miR-3059-5p-inhibited TNFSF15 has been associated with Akt/Erk1/2/Smad2/3-modulated signaling pathway.ConclusionOur results demonstrated a novel finding that BK-c-kit(+) cells enrich exosomal miR-3059-5p to suppress TNFSF15 and promote angiogenesis against hindlimb ischemia in mice.


Persistent Identifierhttp://hdl.handle.net/10722/338255
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.190
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Jingzhou-
dc.contributor.authorSong, Fei-
dc.contributor.authorChen, Ruolan-
dc.contributor.authorYang, Jinjuan-
dc.contributor.authorLiu, Jie-
dc.contributor.authorHuang, Li-
dc.contributor.authorDuan, Fuyu-
dc.contributor.authorKou, Meng-
dc.contributor.authorLian, Boon Xuan-
dc.contributor.authorZhou, Xiaoxia-
dc.contributor.authorHan, Weimin-
dc.contributor.authorMao, Liang-
dc.contributor.authorWu, Chan-
dc.contributor.authorWu, Weiyin-
dc.contributor.authorWei, Rui-
dc.contributor.authorChen, Hao-
dc.contributor.authorXu, Aimin-
dc.contributor.authorTse, Hung-Fat-
dc.contributor.authorLian, Qizhou-
dc.contributor.authorLi, Gang-
dc.contributor.authorWang, Yan-
dc.date.accessioned2024-03-11T10:27:28Z-
dc.date.available2024-03-11T10:27:28Z-
dc.date.issued2023-10-01-
dc.identifier.citationStem Cell Reviews and Reports, 2023, v. 19, n. 7, p. 2481-2496-
dc.identifier.issn2629-3269-
dc.identifier.urihttp://hdl.handle.net/10722/338255-
dc.description.abstract<p>BackgroundProtection of cardiac function following myocardial infarction was largely enhanced by bradykinin-pretreated cardiac-specific c-kit(+) (BK-c-kit(+)) cells, even without significant engraftment, indicating that paracrine actions of BK-c-kit(+) cells play a pivotal role in angiogenesis. Nevertheless, the active components of the paracrine actions of BK-c-kit(+) cells and the underlying mechanisms remain unknown. This study aimed to define the active components of exosomes from BK-c-kit(+) cells and elucidate their underlying protective mechanisms.MethodsMatrigel tube formation assay, cell cycle, and mobility in human umbilical vein endothelial cells (HUVECs) and hindlimb ischemia (HLI) in mice were applied to determine the angiogenic effect of condition medium (CM) and exosomes. Proteome profiler, microRNA sponge, Due-luciferase assay, microRNA-sequencing, qRT-PCR, and Western blot were used to determine the underlying mechanism of the angiogenic effect of exosomes from BK-c-kit(+).ResultsAs a result, BK-c-kit(+) CM and exosomes promoted tube formation in HUVECs and the repair of HLI in mice. Angiogenesis-related proteomic profiling and microRNA sequencing revealed highly enriched miR-3059-5p as a key angiogenic component of BK-c-kit(+) exosomes. Meanwhile, loss- and gain-of-function experiments revealed that the promotion of angiogenesis by miR-3059-5p was mainly through suppression of TNFSF15-inhibited effects on vascular tube formation, cell proliferation and cell migration. Moreover, enhanced angiogenesis of miR-3059-5p-inhibited TNFSF15 has been associated with Akt/Erk1/2/Smad2/3-modulated signaling pathway.ConclusionOur results demonstrated a novel finding that BK-c-kit(+) cells enrich exosomal miR-3059-5p to suppress TNFSF15 and promote angiogenesis against hindlimb ischemia in mice.<br></p>-
dc.languageeng-
dc.publisherSpringer-
dc.relation.ispartofStem Cell Reviews and Reports-
dc.subjectangiogenesis-
dc.subjectBradykinin-
dc.subjectcardiac-specific c-kit+ cells-
dc.subjectexosome-
dc.subjectmiR-3059-5p-
dc.subjectTNFSF15-
dc.titleBradykinin-pretreated Human cardiac-specific c-kit(+) Cells Enhance Exosomal miR-3059-5p and Promote Angiogenesis Against Hindlimb Ischemia in mice-
dc.typeArticle-
dc.identifier.doi10.1007/s12015-023-10591-5-
dc.identifier.pmid37535186-
dc.identifier.scopuseid_2-s2.0-85166647943-
dc.identifier.volume19-
dc.identifier.issue7-
dc.identifier.spage2481-
dc.identifier.epage2496-
dc.identifier.eissn2629-3277-
dc.identifier.isiWOS:001041982200001-
dc.publisher.placeNEW YORK-
dc.identifier.issnl2629-3277-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats