Cortical astroglia undergo transcriptomic dysregulation in the G93A SOD1 ALS mouse model.
Cortical astroglia undergo transcriptomic dysregulation in the G93A SOD1 ALS mouse model.
复制标题
DOI:
10.1080/01677063.2018.1513508
复制
发表时间:
2018-12
影响因子:
1.9
通讯作者:
Rothstein JD
中科院分区:
文献类型:
--
作者:
Miller SJ;Glatzer JC;Hsieh YC;Rothstein JD
Astroglia are the most abundant glia cell in the central nervous system, playing essential roles in maintaining homeostasis. Key functions of astroglia include, but are not limited to, neurotransmitter recycling, ion buffering, immune modulation, neurotrophin secretion, neuronal synaptogenesis and elimination, and blood-brain-barrier maintenance. In neurological diseases, it is well appreciated that astroglia play crucial roles in the disease pathogenesis. In amyotrophic lateral sclerosis (ALS), a motor neuron degenerative disease, astroglia in the spinal cord and cortex downregulate essential transporters, among other proteins, that exacerbate disease progression. Spinal cord astroglia undergo dramatic transcriptome dysregulation. However, in the cortex, it has not been well studied what effects glia, especially astroglia, have on upper motor neurons in the pathology of ALS. To begin to shed light on the involvement and dysregulation that astroglia undergo in ALS, we isolated pure grey-matter cortical astroglia and subjected them to microarray analysis. We uncovered a vast number of genes that show dysregulation at end-stage in the ALS mouse model, G93A SOD1. Many of these genes play essential roles in ion homeostasis and the Wnt-signaling pathway. Several of these dysregulated genes are common in ALS spinal cord astroglia, while many of them are unique. This database serves as an approach for understanding the significance of dysfunctional genes and pathways in cortical astroglia in the context of motor neuron disease, as well as determining regional astroglia heterogeneity, and providing insight into ALS pathogenesis.
登录
查看更多内容
影响因子:
4.2
作者:
Bahadorani, Sepehr;Mukai, Spencer;Hilliker, Arthur J.
通讯作者:
Hilliker, Arthur J.
影响因子:
3.6
作者:
Du, Xiulian;Wang, Qiang;Greene, Mark I.
通讯作者:
Greene, Mark I.
影响因子:
9.9
作者:
ARMON, C;KURLAND, LT;OBRIEN, PC
通讯作者:
OBRIEN, PC
影响因子:
3.8
作者:
Angel, I;Bar, A;Kozak, A
通讯作者:
Kozak, A
DOI:
10.1158/1541-7786.mcr-12-0352
发表时间:
2012-10
期刊:
Molecular cancer research : MCR
影响因子:
--
作者:
Adams SJ;Aydin IT;Celebi JT
通讯作者:
Celebi JT