Protective effects of 7,8-dihydroxyflavone on retinal ganglion and rgc-5 cells against excitotoxic and oxidative stress

Vivek K. Gupta*, Yuyi You, Jonathan C. Li, Alexander Klistorner, Stuart L. Graham

*Corresponding author for this work

    Research output: Contribution to journalArticle

    57 Citations (Scopus)

    Abstract

    A preferential loss of retinal ganglion cells (RGCs) is observed in glaucoma and optic neuritis. Loss of tropomyosin-related kinase receptor B (TrkB)-mediated signaling has been implicated in this degeneration. Our study indicates that 7,8-dihydroxyflavone (7,8 DHF) robustly upregulates the TrkB signaling in the primary rat RGCs and the retinal neuronal precursor RGC-5 cell line by promoting phosphorylation of TrkB receptor, leading to enhanced TrkB receptor tyrosine kinase activity. The flavonoid derivative 7,8 DHF acts a potent TrkB agonist and upregulates the downstream AKT and MAPK/ERK survival signaling pathways in a TrkB-dependent manner in both primary rat RGCs as well as the RGC-5 cell line. Excitotoxicity and oxidative injury have been alleged in the specific RGC degeneration in various forms of glaucoma. A novel finding of this study is that treatment with 7,8 DHF protects these cells significantly from excitotoxic and oxidative stress-induced apoptosis and cell death. 7,8 DHF also promotes neuritogenesis by stimulating neurite outgrowth, suggesting a possible therapeutic strategy for protection of RGCs in various optic neuropathies.

    Original languageEnglish
    Pages (from-to)96-104
    Number of pages9
    JournalJournal of Molecular Neuroscience
    Volume49
    Issue number1
    DOIs
    Publication statusPublished - Jan 2013

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