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.在美国，每年约有12000例新发创伤性脊髓损伤（SCI）病例。目前尚无能够改善脊髓损伤预后的神经保护治疗方案。本团队前期研究证实，在小鼠挫伤性脊髓损伤（contusive spinal cord injury）后，内质网应激反应（ERSR）是引发少突胶质细胞（oligodendrocyte）死亡、继而导致白质丢失与运动功能障碍的关键诱因。内质网应激反应可调控多种转录因子的活性，这些转录因子分别参与调控促存活基因或促凋亡基因的表达。因此，本研究对受内质网应激反应影响的少突胶质细胞进行转录组变化（transcriptomic changes）分析，以此作为识别可缓解脊髓损伤后少突胶质细胞丢失的新型治疗靶点的第一步。