SIRT1 levels appear elevated in human choroidal neovascularization membranes compared with control eyes. Moreover, inhibition of SIRT1 activity is correlated with decreased secretion of potent proangiogenic cytokines. Collectively, these data support a potential role for SIRT1 in the pathogenesis of neovascular age-related macular degeneration.

Compensatory angiogenic signalling may occur in neovascular AMD following treatment with bevacizumab. Here we show that DPE, both alone and in combination with bevacizumab, can reduce the secretion of angiogenin, a cytokine that has been upregulated following treatment with bevacizumab in RPE cells. Therefore, DPE may represent a possible therapeutic agent to be used in combination with bevacizumab for the treatment of neovascular AMD.

Background/Aims: Nuclear receptor corepressor 1 (NCoR1) is a protein complex with diverse functions in development and tumorigenesis. We investigated the pattern of expression and histopathological correlation of NCoR1 in 41 retinoblastoma tumor samples, 1 retinoblastoma cell line (WERI-Rb-1) and human retinal progenitor cells (hRPCs). Methods: Tissue sections from 41 retinoblastoma cases, the retinoblastoma cell line WERI-Rb-1 and hRPCs were stained with rabbit polyclonal anti-NCoR1 H76 antibody. Percentage and intensity of staining were classified by an ocular pathologist from 0 to 3. The paired t test was used to test for differences. Results: In the nonneoplastic retina, NCoR1 was expressed mainly in cell nuclei. The retinoblastoma tumor cells similarly had nuclear NCoR1 but also had a higher level of cytoplasmic NCoR1 expression compared to all 3 normal retinal cell layers (p < 0.002). In contrast to the normal retina, NCoR1 was mainly expressed in the cytoplasm of the proliferating WERI-Rb-1 cells. This cytoplasmic expression pattern was also seen in the undifferentiated hRPCs. Conclusions: The aberrant cytoplasmic expression of NCoR1 in retinoblastoma appears to be associated with the proliferative and/or dedifferentiated properties of retinoblastoma. Further investigation into the role of NCoR1 in retinoblastoma may provide insight into how therapeutically inhibiting its nucleocytoplasmic shuttling may affect retinoblastoma tumor biology.