May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Neuroprotection of Vegf-b by Inhibition of Apoptosis
Author Affiliations & Notes
  • F. Zhang
    NEI/NIH, Bethesda, Maryland
  • Y. Li
    NEI/NIH, Bethesda, Maryland
  • Z. Tang
    NEI/NIH, Bethesda, Maryland
  • N. Nagai
    Kinki University School of Medicine, Department of Physiology, Ohnohigashi 377-2, Osakasayama, Osaka, Japan
  • C.-H. Heldin
    Uppsala University, Ludwig Institute for Cancer Research, Uppsala, Sweden
  • X. Li
    NEI/NIH, Bethesda, Maryland
  • Footnotes
    Commercial Relationships  F. Zhang, None; Y. Li, None; Z. Tang, None; N. Nagai, None; C. Heldin, None; X. Li, None.
  • Footnotes
    Support  National Glaucoma Research
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4945. doi:
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    • Get Citation

      F. Zhang, Y. Li, Z. Tang, N. Nagai, C.-H. Heldin, X. Li; Neuroprotection of Vegf-b by Inhibition of Apoptosis. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4945. doi:

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : the potential neuroprotective effect of VEGF-B.

Methods: : real-time PCR analysis; the NMDA-induced retina injury model and the middle cerebral artery occlusion (MCAO)-induced brain ischemia model

Results: : Indeed, intravitreal (IV) administration of VEGF-B protein rescued the retinal neuronal cells from apoptosis in all the three neuronal layers in the retina. Moreover, VEGF-B protein treatment in the brain decreased stroke volume in the MCAO model, indicating that VEGF-B is a potent neuroprotective factor. Using real-time PCR analysis, we found that VEGF-B inhibits the expression of the BH3-only protein and other apoptotic/cell death-related genes in both the retinae and the brain.

Conclusions: : Taken together, our data have shown that VEGF-B is a potent neuroprotective factor and may potentially offer a new therapeutic option for the treatment of ocular neurodegenerative diseases.

Keywords: neuroprotection • vascular endothelial growth factor • apoptosis/cell death 

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