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Histone deacetylase inhibition-mediated differentiation of RGC-5 cells and interaction with survival. | LitMetric

Histone deacetylase inhibition-mediated differentiation of RGC-5 cells and interaction with survival.

Invest Ophthalmol Vis Sci

Department of Ophthalmology and Visual Sciences, University of Wisconsin Medical School, Madison, Wisconsin 53792, USA.

Published: June 2007

AI Article Synopsis

  • The acetylation of histones, regulated by HDAC and acetyltransferases, plays a key role in gene transcription and neuronal differentiation, which was explored using the RGC-5 cell line.
  • RGC-5 cells were treated with various agents, including trichostatin A (TSA), to evaluate their effects on cell differentiation, neuritogenesis, and transcriptional dependence.
  • The findings indicated that while TSA promoted significant differentiation and neuritogenesis, there were distinct differences between the effects of HDAC inhibition and staurosporine, particularly in terms of the cells' dependence on neurotrophic factors.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2206540PMC
http://dx.doi.org/10.1167/iovs.06-1364DOI Listing

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