May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
VEFG-B Inhibits Oxidative Stress, Serum Deprivation, and Bmf Induced Apoptosis in Cultured Cells
Author Affiliations & Notes
  • X. Hou
    NEI/NIH, Bethesda, Maryland
  • Y. Li
    NEI/NIH, Bethesda, Maryland
  • F. Zhang
    NEI/NIH, Bethesda, Maryland
  • Z. Tang
    NEI/NIH, Bethesda, Maryland
  • C.-H. Heldin
    Uppsala University, Ludwig Institute for Cancer Research, SE-751 24 Uppsala, Sweden
  • X. Li
    NEI/NIH, Bethesda, Maryland
  • Footnotes
    Commercial Relationships  X. Hou, None; Y. Li, None; F. Zhang, None; Z. Tang, None; C. Heldin, None; X. Li, None.
  • Footnotes
    Support  the National Glaucoma Research
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4947. doi:
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      X. Hou, Y. Li, F. Zhang, Z. Tang, C.-H. Heldin, X. Li; VEFG-B Inhibits Oxidative Stress, Serum Deprivation, and Bmf Induced Apoptosis in Cultured Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4947. doi:

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

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Purpose: : to test whether VEGF-B could inhibit apoptosis in the cultured RGC5 cells.

Methods: : We first treated the RGC5 cells with hydrogen peroxide (H2O2), which is known to induce oxidative stress-induced apoptosis, and investigated the apoptosis status using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. VEGF-B167 treatment (100 ng/ml) significantly decreased the H2O2-induced apoptosis in the RGC5 cells by about 50% (n=3, P<0.01). We next tested whether VEGF-B could inhibit the serum deprivation-induced cell death in the RGC5 cells. We cultured the cells in serum-free medium and treated the cells with recombinant proteins of human VEGF-B167 (100 ng/ml), VEGF (25 and 100 ng/ml) and PlGF (25 and 100 ng/ml), and the viability of the cells measured at different time point using the MTT assay. VEGF-B treatment significantly increased cell survival as potently as 10% FCS at day one and two (n=3, P<0.01). The survival effect of VEGF-B167 on the RGC5 cells was slightly greater in a hypoxic condition.

Results: : Bmf is an essential apoptosis inducer in response to cellular stresse. Over-expression of Bmf led to cellular apoptosis within twenty-four hours. The potent inhibitory effect of VEGF-B on the expression of Bmf indicates that VEGF-B may inhibit Bmf-mediated apoptosis. To test this, we overexpressed the mouse Bmf gene in the rat RGC5 cells, and determined the apoptosis rate and the expression of Bmf level in the cells with or without VEGF-B treatment. Bmf overexpression induced significantly cellular apoptosis in the RGC5 cells (n=3, P<0.01). VEGF-B167 treatment (100 ng/ml for forty-eight hours) inhibited the Bmf-induced apoptosis by about 40% (n=3, P<0.01). Further, VEGF-B treatment inhibited the expression of both the endogenous rat and the exogenous mouse Bmf genes (n=3, P<0.01).

Conclusions: : our data have shown that VEGF-B is a potent survival factor for the RGC5 cells by inhibiting the oxidative stress-, serum deprivation-, and Bmf-induced apoptosis.

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

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