Effect of chromogranin A-derived vasostatin-1 on laser-induced choroidal neovascularization in the mouse

Silvia Maestroni, Anna Maestroni, Simona Ceglia, Gemma Tremolada, Monica Mancino, Angelina Sacchi, Rosangela Lattanzio, Ilaria Zucchiatti, Angelo Corti, Francesco Bandello, Gianpaolo Zerbini

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Purpose To verify the effect of vasostatin-1 (VS-1), an anti-angiogenic fragment of chromogranin A, in the prevention of choroidal neovascularization (CNV) in an established mouse model of laser-induced ocular neovascularization. Methods Bruch's membrane, the innermost layer of the choroid, was broken by laser photocoagulation in C57/Bl6 mice, to induce CNV. Mice were then treated daily for 14 days by intraperitoneal injection of VS-1 or vehicle (6 mice/group). CNV and vascular leakage were measured at three time-points (day 0, 7 and 14) in vivo by spectral domain optical coherence tomography (OCT) and fluorescein angiography (FA). Ex vivo analysis of CNV was also performed at day 14 by confocal microscopy analysis of dextran-perfused choroidal flat-mounts. Results In vivo analyses showed that VS-1 significantly reduced CNV at day 14 (p = 0.03) and vascular leakage at day 7 (p = 0.01) and 14 (p = 0.04). Ex vivo confocal microscopy analysis of CNV performed on dextran-perfused choroidal flat-mounts at day 14 confirmed the protective activity of VS-1 (p = 0.01). A significant correlation between the results of in vivo and ex vivo analyses of CNV was also observed (p = 0.001, R2 = 0.81). Conclusion The results indicate that VS-1 can prevent CNV and vascular leakage in a mouse model of ocular neovascularization, suggesting that this polypeptide might have therapeutic activity in human ocular diseases that are complicated by neovascularization or excessive vascular permeability.

Original languageEnglish
Pages (from-to)e218-e222
JournalActa Ophthalmologica
Volume93
Issue number3
DOIs
Publication statusPublished - May 1 2015

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Chromogranin A
Choroidal Neovascularization
Lasers
Blood Vessels
Dextrans
Confocal Microscopy
Bruch Membrane
Choroid
Eye Diseases
vasostatin I
Fluorescein Angiography
Light Coagulation
Optical Coherence Tomography
Capillary Permeability
Intraperitoneal Injections
Human Activities
Peptides

Keywords

  • mouse model
  • ocular neovascularization
  • ophthalmic coherence tomography
  • vasostatin-1

ASJC Scopus subject areas

  • Ophthalmology
  • Medicine(all)

Cite this

Effect of chromogranin A-derived vasostatin-1 on laser-induced choroidal neovascularization in the mouse. / Maestroni, Silvia; Maestroni, Anna; Ceglia, Simona; Tremolada, Gemma; Mancino, Monica; Sacchi, Angelina; Lattanzio, Rosangela; Zucchiatti, Ilaria; Corti, Angelo; Bandello, Francesco; Zerbini, Gianpaolo.

In: Acta Ophthalmologica, Vol. 93, No. 3, 01.05.2015, p. e218-e222.

Research output: Contribution to journalArticle

Maestroni, Silvia ; Maestroni, Anna ; Ceglia, Simona ; Tremolada, Gemma ; Mancino, Monica ; Sacchi, Angelina ; Lattanzio, Rosangela ; Zucchiatti, Ilaria ; Corti, Angelo ; Bandello, Francesco ; Zerbini, Gianpaolo. / Effect of chromogranin A-derived vasostatin-1 on laser-induced choroidal neovascularization in the mouse. In: Acta Ophthalmologica. 2015 ; Vol. 93, No. 3. pp. e218-e222.
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AU - Maestroni, Anna

AU - Ceglia, Simona

AU - Tremolada, Gemma

AU - Mancino, Monica

AU - Sacchi, Angelina

AU - Lattanzio, Rosangela

AU - Zucchiatti, Ilaria

AU - Corti, Angelo

AU - Bandello, Francesco

AU - Zerbini, Gianpaolo

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N2 - Purpose To verify the effect of vasostatin-1 (VS-1), an anti-angiogenic fragment of chromogranin A, in the prevention of choroidal neovascularization (CNV) in an established mouse model of laser-induced ocular neovascularization. Methods Bruch's membrane, the innermost layer of the choroid, was broken by laser photocoagulation in C57/Bl6 mice, to induce CNV. Mice were then treated daily for 14 days by intraperitoneal injection of VS-1 or vehicle (6 mice/group). CNV and vascular leakage were measured at three time-points (day 0, 7 and 14) in vivo by spectral domain optical coherence tomography (OCT) and fluorescein angiography (FA). Ex vivo analysis of CNV was also performed at day 14 by confocal microscopy analysis of dextran-perfused choroidal flat-mounts. Results In vivo analyses showed that VS-1 significantly reduced CNV at day 14 (p = 0.03) and vascular leakage at day 7 (p = 0.01) and 14 (p = 0.04). Ex vivo confocal microscopy analysis of CNV performed on dextran-perfused choroidal flat-mounts at day 14 confirmed the protective activity of VS-1 (p = 0.01). A significant correlation between the results of in vivo and ex vivo analyses of CNV was also observed (p = 0.001, R2 = 0.81). Conclusion The results indicate that VS-1 can prevent CNV and vascular leakage in a mouse model of ocular neovascularization, suggesting that this polypeptide might have therapeutic activity in human ocular diseases that are complicated by neovascularization or excessive vascular permeability.

AB - Purpose To verify the effect of vasostatin-1 (VS-1), an anti-angiogenic fragment of chromogranin A, in the prevention of choroidal neovascularization (CNV) in an established mouse model of laser-induced ocular neovascularization. Methods Bruch's membrane, the innermost layer of the choroid, was broken by laser photocoagulation in C57/Bl6 mice, to induce CNV. Mice were then treated daily for 14 days by intraperitoneal injection of VS-1 or vehicle (6 mice/group). CNV and vascular leakage were measured at three time-points (day 0, 7 and 14) in vivo by spectral domain optical coherence tomography (OCT) and fluorescein angiography (FA). Ex vivo analysis of CNV was also performed at day 14 by confocal microscopy analysis of dextran-perfused choroidal flat-mounts. Results In vivo analyses showed that VS-1 significantly reduced CNV at day 14 (p = 0.03) and vascular leakage at day 7 (p = 0.01) and 14 (p = 0.04). Ex vivo confocal microscopy analysis of CNV performed on dextran-perfused choroidal flat-mounts at day 14 confirmed the protective activity of VS-1 (p = 0.01). A significant correlation between the results of in vivo and ex vivo analyses of CNV was also observed (p = 0.001, R2 = 0.81). Conclusion The results indicate that VS-1 can prevent CNV and vascular leakage in a mouse model of ocular neovascularization, suggesting that this polypeptide might have therapeutic activity in human ocular diseases that are complicated by neovascularization or excessive vascular permeability.

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