Transcriptional control of retinal ganglion cell death after axonal injury

Purpose: This study aims to the downstream transcriptional networks controlled by JUN and DDIT which are critical for RGC death Methods: RNA was isolated from the retinas of wild-type mice and mice deficient in Jun, Ddit3, and both Jun and Ddit3 three days after mechanical optic nerve crush injury (CONC), and was subjected to RNA-sequecing. Results: This study identified downstream transcriptional changes after injury included both neuronal survival and pro-inflammatory signaling that were attenuated to differing degrees by loss of Ddit3, Jun, and Ddit3/Jun. Conclusion: These data suggest pro-inflammatory signaling in the retina might be secondary to activation of pro-death pathways in RGCs after acute axonal injury. These results determine the downstream transcriptional networks important for apoptotic signaling which may be important for ordering and staging the pro-degenerative signals after mechanical axonal injury. Overall design: Retina mRNA profiles of wild-type and mice deficient in Jun (Jun-/-), Ddit3 (Ddit3-/-), and both Jun and Ddit3 (Jun-/- Ddit3-/-) three days after mechanical optic nerve crush injury (CONC)