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Apatinib, an Inhibitor of Vascular Endothelial Growth Factor Receptor 2, Suppresses Pathologic Ocular Neovascularization in Mice.

Abstract Vascular endothelial growth factor (VEGF) signaling via VEGF receptor 2 (VEGFR2) plays a crucial role in pathologic ocular neovascularization. In this study, we investigated the antiangiogenic effect of apatinib, a pharmacologic inhibitor of VEGFR2 tyrosine kinase, against oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) in mice.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title investigative ophthalmology & visual science
Publication Year Start




PMID- 28715845
OWN - NLM
STAT- In-Process
DA  - 20170717
LR  - 20170717
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 58
IP  - 9
DP  - 2017 Jul 01
TI  - Apatinib, an Inhibitor of Vascular Endothelial Growth Factor Receptor 2,
      Suppresses Pathologic Ocular Neovascularization in Mice.
PG  - 3592-3599
LID - 10.1167/iovs.17-21416 [doi]
AB  - Purpose: Vascular endothelial growth factor (VEGF) signaling via VEGF receptor 2 
      (VEGFR2) plays a crucial role in pathologic ocular neovascularization. In this
      study, we investigated the antiangiogenic effect of apatinib, a pharmacologic
      inhibitor of VEGFR2 tyrosine kinase, against oxygen-induced retinopathy (OIR) and
      laser-induced choroidal neovascularization (CNV) in mice. Methods: Western
      blotting and in vitro angiogenesis assays were performed using human retinal
      microvascular endothelial cells (HRMECs). OIR was induced in neonatal mice by
      exposure to 75% oxygen from postnatal day (P) 7 to P12 and to room air from P12
      to P17. Experimental CNV was induced in mice using laser photocoagulation.
      Apatinib was intravitreally and orally administered to mice. Neovascularization
      and phosphorylation of VEGFR2 were evaluated by immunofluorescence staining.
      Results: Apatinib inhibited VEGF-mediated activation of VEGFR2 signaling and
      substantially reduced VEGF-induced proliferation, migration, and cord formation
      in HRMECs. A single intravitreal injection of apatinib significantly attenuated
      retinal or choroidal neovascularization in mice with OIR or laser injury-induced 
      CNV, respectively. Retinal or choroidal tissues of the eyes treated with apatinib
      exhibited substantially lower phosphorylation of VEGFR2 than those of controls
      injected with vehicle. Intravitreal injection of apatinib did not cause
      noticeable ocular toxicity. Moreover, oral administration of apatinib
      significantly reduced laser-induced CNV in mice. Conclusions: Our study
      demonstrates that apatinib inhibits pathologic ocular neovascularization in mice 
      with OIR or laser-induced CNV. Apatinib may, therefore, be a promising drug for
      the prevention and treatment of ischemia-induced proliferative retinopathy and
      neovascular age-related macular degeneration.
FAU - Kim, Koung Li
AU  - Kim KL
AD  - College of Pharmacy, Chung-Ang University, Seoul, Korea.
FAU - Suh, Wonhee
AU  - Suh W
AD  - College of Pharmacy, Chung-Ang University, Seoul, Korea.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
EDAT- 2017/07/18 06:00
MHDA- 2017/07/18 06:00
CRDT- 2017/07/18 06:00
AID - 2644895 [pii]
AID - 10.1167/iovs.17-21416 [doi]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2017 Jul 1;58(9):3592-3599. doi:
      10.1167/iovs.17-21416.