Chronic expression of PPAR-delta by oligodendrocyte lineage cells in the injured rat spinal cord

大鼠脊髓损伤中少突胶质细胞系细胞对 PPAR-delta 的慢性表达

阅读:8
作者:Akshata Almad, Dana M McTigue

Abstract

The transcription factor peroxisome proliferator-activated receptor (PPAR)-delta promotes oligodendrocyte differentiation and myelin formation in vitro and is prevalent throughout the brain and spinal cord. Its expression after injury, however, has not been examined. Thus, we used a spinal contusion model to examine the spatiotemporal expression of PPAR-delta in naïve and injured spinal cords from adult rats. As previously reported, PPAR-delta was expressed by neurons and oligodendrocytes in uninjured spinal cords; PPAR-delta was also detected in NG2 cells (potential oligodendrocyte progenitors) within the white matter and gray matter. After spinal cord injury (SCI), PPAR-delta mRNA and protein were present early and increased over time. Overall PPAR-delta+ cell numbers declined at 1 day post injury (dpi), likely reflecting neuron loss, and then rose through 14 dpi. A large proportion of NG2 cells expressed PPAR-delta after SCI, especially along lesion borders. PPAR-delta+ NG2 cell numbers were significantly higher than naive by 7 dpi and remained elevated through at least 28 dpi. PPAR-delta+ oligodendrocyte numbers declined at 1 dpi and then increased over time such that >20% of oligodendrocytes expressed PPAR-delta after SCI compared with approximately 10% in uninjured tissue. The most prominent increase in PPAR-delta+ oligodendrocytes was along lesion borders where at least a portion of newly generated oligodendrocytes (bromodeoxyuridine+) were PPAR-delta+. Consistent with its role in cellular differentiation, the early rise in PPAR-delta+ NG2 cells followed by an increase in new PPAR-delta+ oligodendrocytes suggests that this transcription factor may be involved in the robust oligodendrogenesis detected previously along SCI lesion borders.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。