Abstract: Objective To investigate the mechanism of high transcription of the glial cell-line derived neurotrophic factor (gdnf)
gene induced by hyperacetylation of histone H3 lysine 9 (H3K9) at its promoter region II in rat C6 glioma cells. Methods The
acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and the binding capacity of Egr-1 to its binding
site in gdnf promoter were examined by ChIP-PCR in C6 astroglioma cells and normal rat astrocytes, and its changes were
investigated in C6 astroglioma cells after treatment with histone acetyltransferase inhibitor curcumin or deacetylase inhibitor
trichostatin A. Results Compared normal astrocytes, C6 astroglioma cells showed significantly increased acetylation level of
H3K9 at Egr-1 binding site in gdnf gene promoter region II and Egr-1 binding capacity (P<0.01). Curcumin treatment
significantly reduced H3K9 acetylation level at Egr-1 binding site and decreased both the binding of Egr-1 to promoter region
II and gdnf mRNA levels in C6 astroglioma cells (P<0.05). Conversely, increased H3K9 acetylation at the Egr-1 binding site
induced by trichostatin A significantly increased the binding of Egr-1 to promoter region II and gdnf mRNA expression levels
(P<0.05). Conclusion H3K9 hyperacetylation induces increased Egr-1 binding to gdnf gene promoter II, which might be the
reason for the high transcription level of gdnf gene in rat C6 glioma cells.