Inhibition of Choroidal and Corneal Pathologic Neovascularization by Plgf1-de Gene Transfer. (Articolo in rivista)

Type
Label
  • Inhibition of Choroidal and Corneal Pathologic Neovascularization by Plgf1-de Gene Transfer. (Articolo in rivista) (literal)
Anno
  • 2012-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1167/iovs.12-10658. (literal)
Alternative label
  • Tarallo V, Bogdanovich S, Hirano Y, Tudisco L, Zentilin L, Giacca M, Ambati J, De Falco S. (2012)
    Inhibition of Choroidal and Corneal Pathologic Neovascularization by Plgf1-de Gene Transfer.
    in Investigative ophthalmology & visual science
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Tarallo V, Bogdanovich S, Hirano Y, Tudisco L, Zentilin L, Giacca M, Ambati J, De Falco S. (literal)
Pagina inizio
  • 7989 (literal)
Pagina fine
  • 7996 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 53 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 13 (literal)
Note
  • PubMe (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Angiogenesis Lab, Institute of Genetics and Biophysics, CNR, Naples, Italy; Department of Ophthalmology & Visual Sciences, University of Kentucky,Lexington, KY, USA; Molecular Medicine Laboratory, ICGEB, Trieste, Italy. (literal)
Titolo
  • Inhibition of Choroidal and Corneal Pathologic Neovascularization by Plgf1-de Gene Transfer. (literal)
Abstract
  • Ocular neovascularization (NV), the primary cause of blindness, typically is treated via inhibition of VEGF-A activity. However, besides VEGF-A, other proteins of the same family, including VEGF-B and placental growth factor (PlGF, all together VEGFs), have a crucial role in the angiogenesis process. PlGF and VEGF, which form heterodimers if co-expressed, both are required for pathologic angiogenesis. We generated a PlGF1 variant, named PlGF1-DE, which is unable to bind and activate VEGFR-1, but retains the ability to form heterodimer. PlGF1-DE acts as dominant negative of VEGF-A and PlGF1wt through heterodimerization mechanism. The purpose of our study was to explore the therapeutic potential of Plgf1-de gene in choroid and cornea NV context. METHODS: In the model of laser-induced choroidal neovascularization (CNV), Plgf1-de gene, and as control Plgf1wt, LacZ, or gfp genes, were delivered using adeno-associated virus (AAV) vector by subretinal injection 14 days before the injury. After 7 days CNV volume was assessed. Corneal NV was induced by scrape or suture procedures. Expression vectors for PlGF1wt or PlGF1-DE, and as control the empty vector pCDNA3, were injected in the mouse cornea after the vascularization insults. NV was evaluated with CD31 and LYVE-1 immunostaining. RESULTS: The expression of Plgf1-de induced significant inhibition of choroidal and corneal NV by reducing VEGF-A homodimer production. Conversely, the delivery of Plgf1wt, despite induced similar reduction of VEGF-A production, did not affect NV. CONCLUSIONS: Plgf1-de gene is a new therapeutic tool for the inhibition of VEGFs driven ocular NV. (literal)
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