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  • Hao, Xiaojin (författare)

Myocardial angiogenesis after plasmid or adenoviral VEGF-A(165) gene transfer in rat myocardial infarction model

  • Artikel/kapitelEngelska2007

Förlag, utgivningsår, omfång ...

  • Oxford University Press (OUP),2007
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:kth-16381
  • https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-16381URI
  • https://doi.org/10.1016/j.cardiores.2006.10.011DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:1956218URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • QC 20100525
  • Objective: To compare gene transfer of plasmid (P) and adenovirus (Ad) encoding human vascular endothelial growth factor-A(165) (hVEGF-A(165)) angiogenic efficacy and adverse effects as regards apoptosis and ectopic expression of the transgene in a rat myocardial infarction model. Methods: Myocardial infarction was provoked in Fisher rats. One week later, PhVEGF-A(165), PLacZ, AdhVEGF-A(165), or AdLacZ was transferred intramyocardially along the border of the myocardial infarction. hVEGF-A expression was detected with ELISA. Myocardial vessel density was analyzed 1 and 4 weeks after gene transfer. Apoptosis was detected by TUNEL staining. Cardiac function was assessed with Tissue Doppler Velocity Imaging. Results: Although AdhVEGF-A(165) had substantially higher myocardial hVEGF-A expression than PhVEGF-A(165), AdhVEGF-A(165) and PhVEGF-A(165) induced angiogenic effects to a similar extent with maintained increased arteriolar density after 4 weeks of gene transfer (p < 0.05). The two treatments also improved left ventricular function similarly. Adenoviral gene transfer induced a higher number of TUNEL positive cells than plasmid (p < 0.02). Ectopic expression of the transgene was present with both vectors but substantially higher after adenoviral gene transfer. Conclusions: AdhVEGF-A165 has no obvious angiogenic advantage over PhVEGF-A165 but more side effects at least in a rat myocardial infarction model. This indicates that PhVEGF-A(165) might be more applicable for therapeutic angiogenesis than AdhVEGF-A(165).

Ämnesord och genrebeteckningar

  • angiogenesis
  • gene therapy
  • infarction
  • growth factors
  • apoptosis
  • endothelial growth-factor
  • expression
  • ischemia
  • vectors
  • feasibility
  • mechanisms
  • apoptosis
  • therapy
  • artery
  • trial

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Mansson-Broberg, AgnetaKarolinska Institutet (författare)
  • Grinnemo, Karl-HenrikKarolinska Institutet (författare)
  • Siddiqui, Anwar J.Karolinska Institutet (författare)
  • Dellgren, Goran (författare)
  • Brodin, Lars-ÅkeKarolinska Institutet(Swepub:kth)u1jq9s27 (författare)
  • Sylven, ChristerKarolinska Institutet (författare)
  • Karolinska Institutet (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Cardiovascular Research: Oxford University Press (OUP)73:3, s. 481-4870008-63631755-3245

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