http://www.cnr.it/ontology/cnr/individuo/prodotto/ID304679
Protective effects of Beta1/2 adrenergic receptor deletion in a model of oxygen-induced retinopathy (Articolo in rivista)
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- 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)
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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)
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- Dal Monte, M., Cammalleri, M., Mattei, E., Filippi, L., Bagnoli, P. (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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