PubMed ID: 17525221
Author(s): Schwechter BR, Millet LE, Levin LA. Histone deacetylase inhibition-mediated differentiation of RGC-5 cells and interaction with survival. Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2845-57. PMID 17525221
Journal: Investigative Ophthalmology & Visual Science, Volume 48, Issue 6, Jun 2007
PURPOSE The acetylation state of histones is modulated by histone deacetylase (HDAC) and histone acetyltransferase and is an important component in regulating gene transcription, including neuronal differentiation. The authors studied the relationship between histone acetylation and the differentiation and survival of the RGC-5 cell line and compared it with nontranscriptional-dependent differentiation with staurosporine.
METHODS The retinal ganglion cell line RGC-5 was treated with trichostatin A (TSA), other HDAC inhibitors, and staurosporine; differentiation, neuritogenesis, neurotrophic factor dependence, and dependence on RNA transcription were assessed.
RESULTS TSA caused significant differentiation and neuritogenesis. Differences between HDAC inhibition and staurosporine differentiation included the proportion of differentiated cells, cell viability, cell morphology, and transcriptional dependence. HDAC inhibition, but not staurosporine differentiation, resulted in RGC-5 cells that were neurotrophic factor dependent.
CONCLUSIONS These results implicate two different mechanisms for RGC-5 differentiation, with a common downstream effect on neurite outgrowth but a differential effect on neurotrophic factor dependence.