Protective effects of Beta1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy (Articolo in rivista)

Type
Label
  • Protective effects of Beta1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1167/iovs.14-15263 (literal)
Alternative label
  • Dal Monte, M., Cammalleri, M., Mattei, E., Filippi, L., Bagnoli, P. (2014)
    Protective effects of Beta1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy
    in Investigative ophthalmology & visual science; ARVO, The association for research in vision and ophthalmology, Rockville [Md.] (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Dal Monte, M., Cammalleri, M., Mattei, E., Filippi, L., Bagnoli, P. (literal)
Pagina inizio
  • 59 (literal)
Pagina fine
  • 73 (literal)
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  • http://intl.iovs.org (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • Dec 11;56 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 15 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 1 (literal)
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  • Massimo Dal Monte - Department of Biology, University of Pisa, Pisa, Italy Maurizio Cammalleri - Department of Biology, University of Pisa, Pisa, Italy Paola Bagnoli - Department of Biology, University of Pisa, Pisa, Italy Elisabetta Mattei - Institute of Neurobiology and Molecular Biology, CNR -IRCCS Fondazione Santa Lucia, Rome, Italy Luca Filippi - Neonatal Intensive Care Unit, Medical Surgical Fetal-Neonatal Department, \"A. Meyer\" University Children's Hospital, Florence, Italy Luca Filippi4 and (literal)
Titolo
  • Protective effects of Beta1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy (literal)
Abstract
  • Purpose. beta-adrenergic receptors (beta-ARs) regulate angiogenesis in proliferative retinopathies. We studied the effects of beta1/2-AR deletion in a model of oxygen-induced retinopathy (OIR) to confirm the role of beta1- and/or beta2-ARs in regulating angiogenesis and to get insights into the role of beta3-ARs. Methods. Mice with beta1/2-AR deletion (KO) were used. Levels of norepinephrine (NE), beta3-ARs, transcription, and proangiogenic factors were evaluated. Retinas were analyzed for avascular area and neovascular tufts in the superficial plexus. Deep plexus and blood-retinal barrier (BRB) were also analyzed. Neovascularization, proangiogenic factors, protein kinase A (PKA) activity, and nitrite production were assessed after BRL 37344, a beta3-AR agonist. Results. Oxygen-induced retinopathy was characterized by NE upregulation with higher levels in wild type (WT) than in KO. Wild type and KO displayed comparable levels of beta3-ARs, transcription, and proangiogenic factors, but differed in VEGF receptor (VEGFR) expression with VEGFR-1 in WT lower than in KO and VEGFR-2 in WT higher than in KO. Blood-retinal barrier dysfunction did not differ between WT and KO. Vascular abnormalities in the superficial plexus were abolished by beta1/2-AR deletion, which also helped the development of the deep plexus. In both WT and KO, beta3-AR agonism, acting through the nitric oxide pathway, caused enhanced neovascular responses with increased levels of VEGF. Conclusions. We confirm that beta1- and beta2-ARs play a pivotal role in retinal angiogenesis. In their presence, bea3-ARs potentiate angiogenic responses, whereas, in their absence, beta3-ARs sustain the angiogenic drive. These results suggest beta-ARs as promising targets for therapies aimed to counteract proliferative retinopathies. (literal)
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