Transcriptome response to endoplasmic reticulum stress in rat oligodendrocyte precursor cells

In the US, there are approximately 12,000 new cases of traumatic spinal cord injury (SCI) each year. Currently there are no neuroprotective treatments to improve outcome of SCI. Our previous research has revealed that endoplasmic reticulum stress response (ERSR) is an important contributor to oligodendrocyte death and subsequent white matter loss and locomotor impairment after contusive spinal cord injury in mice. ERSR affects activity of multiple transcription factors regulating either pro-survival- or apoptosis-promoting genes. Therefore, we characterized transcriptomic changes in ERSR-challenged oligodendrocytes as a first step to identify new targets for therapies that may attenuate their loss after SCI. Total RNA for library construction was obtained from cultured rat oligodendrocyte precursor cells (OPCs) which are often used as a convenient model of oligodendrocytes. These cells were originally isolated from adult rat spinal cords by our collaborator Dr. Scott Whittemore. Only low passage cells were used (up to passage 6). OPCs were treated with the ERSR inducer tunicamycin (0 or 5 µM) for 2- or 8h (4 samples from each experiment, 3 independent experiments were analyzed resulting in 12 samples, total). The two time points selected (both preceding cell death) were used to increase the probability of identifying important transcriptomic components of the ERSR that determine its outcome on oligodendrocyte survival.