Expression and Activity of the Na-K ATPase in Ischemic Injury of Primary Cultured Astrocytes.
10.4196/kjpp.2013.17.4.275
- Author:
Mi Jung KIM
1
;
Jinyoung HUR
;
In Hye HAM
;
Hye Jin YANG
;
Younghoon KIM
;
Seungjoon PARK
;
Young Wuk CHO
Author Information
1. Department of Physiology, Biomedical Science Institute and Medical Research Center, School of Medicine, Kyung Hee University, Seoul 130-701, Korea. ywcho@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Chemical ischemia;
Na-K ATPase;
Primary cultured astrocytes
- MeSH:
Adenosine Triphosphatases;
Astrocytes;
Brain Injuries;
Glucose;
Ischemia;
L-Lactate Dehydrogenase;
Neuroglia;
Neurons;
RNA, Messenger;
Sodium Azide
- From:The Korean Journal of Physiology and Pharmacology
2013;17(4):275-281
- CountryRepublic of Korea
- Language:English
-
Abstract:
Astrocytes are reported to have critical functions in ischemic brain injury including protective effects against ischemia-induced neuronal dysfunction. Na-K ATPase maintains ionic gradients in astrocytes and is suggested as an indicator of ischemic injury in glial cells. Here, we examined the role of the Na-K ATPase in the pathologic process of ischemic injury of primary cultured astrocytes. Chemical ischemia was induced by sodium azide and glucose deprivation. Lactate dehydrogenase assays showed that the cytotoxic effect of chemical ischemia on astrocytes began to appear at 2 h of ischemia. The expression of Na-K ATPase alpha1 subunit protein was increased at 2 h of chemical ischemia and was decreased at 6 h of ischemia, whereas the expression of alpha1 subunit mRNA was not changed by chemical ischemia. Na-K ATPase activity was time-dependently decreased at 1, 3, and 6 h of chemical ischemia, whereas the enzyme activity was temporarily recovered to the control value at 2 h of chemical ischemia. Cytotoxicity at 2 h of chemical ischemia was significantly blocked by reoxygenation for 24 h following ischemia. Reoxygenation following chemical ischemia for 1 h significantly increased the activity of the Na-K ATPase, while reoxygenation following ischemia for 2 h slightly decreased the enzyme activity. These results suggest that the critical time for ischemia-induced cytotoxicity of astrocytes might be 2 h after the initiation of ischemic insult and that the increase in the expression and activity of the Na-K ATPase might play a protective role during ischemic injury of astrocytes.
