File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Modified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarction

TitleModified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarction
Authors
Issue Date2013
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nbt
Citation
Nature Biotechnology, 2013, v. 31 n. 10, p. 898-907 How to Cite?
AbstractIn a cell-free approach to regenerative therapeutics, transient application of paracrine factors in vivo could be used to alter the behavior and fate of progenitor cells to achieve sustained clinical benefits. Here we show that intramyocardial injection of synthetic modified RNA (modRNA) encoding human vascular endothelial growth factor-A (VEGF-A) results in the expansion and directed differentiation of endogenous heart progenitors in a mouse myocardial infarction model. VEGF-A modRNA markedly improved heart function and enhanced long-term survival of recipients. This improvement was in part due to mobilization of epicardial progenitor cells and redirection of their differentiation toward cardiovascular cell types. Direct in vivo comparison with DNA vectors and temporal control with VEGF inhibitors revealed the greatly increased efficacy of pulse-like delivery of VEGF-A. Our results suggest that modRNA is a versatile approach for expressing paracrine factors as cell fate switches to control progenitor cell fate and thereby enhance long-term organ repair.
Persistent Identifierhttp://hdl.handle.net/10722/195540
ISSN
2015 Impact Factor: 43.113
2015 SCImago Journal Rankings: 18.932
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZangi, L-
dc.contributor.authorLui, KO-
dc.contributor.authorvon Gise, A-
dc.contributor.authorMa, Q-
dc.contributor.authorEbina, W-
dc.contributor.authorPtaszek, LM-
dc.contributor.authorSpäter, D-
dc.contributor.authorXu, H-
dc.contributor.authorTabebordbar, M-
dc.contributor.authorGorbatov, R-
dc.contributor.authorSena, B-
dc.contributor.authorNahrendorf, M-
dc.contributor.authorBriscoe, DM-
dc.contributor.authorLi, RA-
dc.contributor.authorWagers, AJ-
dc.contributor.authorRossi, DJ-
dc.contributor.authorPu, WT-
dc.contributor.authorChien, KR-
dc.date.accessioned2014-03-03T08:28:10Z-
dc.date.available2014-03-03T08:28:10Z-
dc.date.issued2013-
dc.identifier.citationNature Biotechnology, 2013, v. 31 n. 10, p. 898-907-
dc.identifier.issn1087-0156-
dc.identifier.urihttp://hdl.handle.net/10722/195540-
dc.description.abstractIn a cell-free approach to regenerative therapeutics, transient application of paracrine factors in vivo could be used to alter the behavior and fate of progenitor cells to achieve sustained clinical benefits. Here we show that intramyocardial injection of synthetic modified RNA (modRNA) encoding human vascular endothelial growth factor-A (VEGF-A) results in the expansion and directed differentiation of endogenous heart progenitors in a mouse myocardial infarction model. VEGF-A modRNA markedly improved heart function and enhanced long-term survival of recipients. This improvement was in part due to mobilization of epicardial progenitor cells and redirection of their differentiation toward cardiovascular cell types. Direct in vivo comparison with DNA vectors and temporal control with VEGF inhibitors revealed the greatly increased efficacy of pulse-like delivery of VEGF-A. Our results suggest that modRNA is a versatile approach for expressing paracrine factors as cell fate switches to control progenitor cell fate and thereby enhance long-term organ repair.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nbt-
dc.relation.ispartofNature Biotechnology-
dc.titleModified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarctionen_US
dc.typeArticleen_US
dc.identifier.emailLi, RA: ronaldli@HKUCC.hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/nbt.2682-
dc.identifier.pmid24013197-
dc.identifier.hkuros239623-
dc.identifier.volume31-
dc.identifier.issue10-
dc.identifier.spage898-
dc.identifier.epage907-
dc.identifier.isiWOS:000325541300018-
dc.publisher.placeUnited States-
dc.identifier.f1000718102305-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats