Journal
GLIA
Volume 62, Issue 7, Pages 1162-1175Publisher
WILEY
DOI: 10.1002/glia.22671
Keywords
proliferation; migration; sodium channels; sodium-calcium exchanger; glial scar
Categories
Funding
- National Institute of General Medical Studies, National Institutes of Health [NGM007205]
- Rehabilitation Research Service and Medical Research Service
- Department of Veterans Affairs
Ask authors/readers for more resources
Astrogliosis is a prominent feature of many, if not all, pathologies of the brain and spinal cord, yet a detailed understanding of the underlying molecular pathways involved in the transformation from quiescent to reactive astrocyte remains elusive. We investigated the contribution of voltage-gated sodium channels to astrogliosis in an in vitro model of mechanical injury to astrocytes. Previous studies have shown that a scratch injury to astrocytes invokes dual mechanisms of migration and proliferation in these cells. Our results demonstrate that wound closure after mechanical injury, involving both migration and proliferation, is attenuated by pharmacological treatment with tetrodotoxin (TTX) and KB-R7943, at a dose that blocks reverse mode of the Na+/Ca2+ exchanger (NCX), and by knockdown of Na(v)1.5 mRNA. We also show that astrocytes display a robust [Ca2+](i) transient after mechanical injury and demonstrate that this [Ca2+](i) response is also attenuated by TTX, KB-R7943, and Na(v)1.5 mRNA knockdown. Our results suggest that Na(v)1.5 and NCX are potential targets for modulation of astrogliosis after injury via their effect on [Ca2+](i). GLIA 2014;62:1162-1175
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available