An augmentation in histone dimethylation at lysine nine residues elicits vision impairment following traumatic brain injury.

ABSTRACT: Traumatic Brain Injury (TBI) affects more than 1.7 million Americans each year and about 30% of TBI-patients having visual impairments. The loss of retinal ganglion cells (RGC) in the retina and axonal degeneration in the optic nerve have been attributed to vision impairment following TBI; however, the molecular mechanism has not been elucidated. Here we have shown that an increase in histone di-methylation at lysine 9 residue (H3K9Me2), synthesized by the catalytic activity of a histone methyltransferase, G9a is responsible for RGC loss and axonal degeneration in the optic nerve following TBI. To elucidate the molecular mechanism, we found that an increase in H3K9Me2 results in the induction of oxidative stress both in the RGC and optic nerve by decreasing the mRNA level of antioxidants s

SUBMITTER: Gupta R 

PROVIDER: S-EPMC6588499 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature