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. 2015 May 6;2:15013. doi: 10.1038/mtm.2015.13

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Copyright © 2015 American Society of Gene & Cell Therapy

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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Silencing p75^NTR suppresses proNGF-induced vascular cell death and apoptotic marker in rat retina. Representative images of trypsin-digested retinas stained with TUNEL (green) and counterstained with DAPI (blue) are shown for (a) GFP+Scr, (b) GFP+p75shRNA, (c) proNGF+Scr, and (d) proNGF+p75shRNA. TUNEL assay showed several positive cells in proNGF-overexpressing retinas, suggesting that capillary degradation occurs through apoptosis. (e) Representative western blots and statistical analysis of pJNK and JNK and (f) cleaved-PARP normalized to actin. 2 × 2 analysis showed interaction between proNGF expression and silencing p75^NTR. Overexpression of proNGF induced significant activation of JNK and cleavage of PARP compared with GFP-controls. These effects were mitigated by p75shRNA but not scrambled. Results presented as mean ± SD. n = 4–6 per group. *P < 0.05 versus other groups.