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Tumor necrosis factor-α promotes the expression of excitatory amino-acid transporter 2 in astrocytes: Optimal concentration and incubation time.

Ding Y, Zhang K, Liu S, Zhang Q, Ma C, Bruce IC, Zhang X - Exp Ther Med (2014)

Bottom Line: The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia.The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change.The present results suggest that a relatively short-term application of an optimal concentration of TNF-α may protect neurons against ischemic injury by elevating the expression of EAAT2 in astrocytes.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Zhejiang University City College, Hangzhou, Zhejiang 310015, P.R. China ; Department of Basic Medicine, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.

ABSTRACT
The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia. Exogenous TNF-α was administered to pure cultured astrocytes and the expression levels of EAAT1, EAAT2 and glial fibrillary acidic protein (GFAP) were evaluated. The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change. To determine whether the elevation in the levels of the EAAT2 protein induced by TNF-α had a beneficial effect on ischemic insult, TNF-α was applied to in vitro models of cerebral ischemia; the treatment was observed to increase neuronal viability. The present results suggest that a relatively short-term application of an optimal concentration of TNF-α may protect neurons against ischemic injury by elevating the expression of EAAT2 in astrocytes.

No MeSH data available.


Related in: MedlinePlus

Expression levels of EAATs in astrocytes treated with TNF-α for different time-periods. (A) Representative western blot analysis of EAAT1, EAAT2, GFAP and β-actin. (B) Densitometric analysis showing the expression levels of the EAATs or GFAP normalized to β-actin. Data are presented as the mean ± standard deviation (n=6). **P<0.01 compared with the control group (prior to TNF-α treatment, 0 h). TNF-α, tumor necrosis factor-α; EAAT, excitatory amino-acid transporter; GFAP, glial fibrillary acidic protein.
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f3-etm-08-06-1909: Expression levels of EAATs in astrocytes treated with TNF-α for different time-periods. (A) Representative western blot analysis of EAAT1, EAAT2, GFAP and β-actin. (B) Densitometric analysis showing the expression levels of the EAATs or GFAP normalized to β-actin. Data are presented as the mean ± standard deviation (n=6). **P<0.01 compared with the control group (prior to TNF-α treatment, 0 h). TNF-α, tumor necrosis factor-α; EAAT, excitatory amino-acid transporter; GFAP, glial fibrillary acidic protein.

Mentions: To further explore the association between incubation time and the expression levels of EAATs in astrocytes, the astrocytes were treated with the optimal concentration of TNF-α (10 ng/ml) for different incubation periods (4, 8, 12, 24, 36 or 72 h). The EAAT2 protein expression showed a time-dependent increase, followed by a time-dependent decrease, with a maximum level (P<0.01) after 12 h (Fig. 3). However, the expression levels of EAAT1 and GFAP did not change with treatment. These results indicated that short-term treatment with the optimal concentration of TNF-α promoted EAAT2 expression in astrocytes, which was independent of astrocyte proliferation.


Tumor necrosis factor-α promotes the expression of excitatory amino-acid transporter 2 in astrocytes: Optimal concentration and incubation time.

Ding Y, Zhang K, Liu S, Zhang Q, Ma C, Bruce IC, Zhang X - Exp Ther Med (2014)

Expression levels of EAATs in astrocytes treated with TNF-α for different time-periods. (A) Representative western blot analysis of EAAT1, EAAT2, GFAP and β-actin. (B) Densitometric analysis showing the expression levels of the EAATs or GFAP normalized to β-actin. Data are presented as the mean ± standard deviation (n=6). **P<0.01 compared with the control group (prior to TNF-α treatment, 0 h). TNF-α, tumor necrosis factor-α; EAAT, excitatory amino-acid transporter; GFAP, glial fibrillary acidic protein.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4217772&req=5

f3-etm-08-06-1909: Expression levels of EAATs in astrocytes treated with TNF-α for different time-periods. (A) Representative western blot analysis of EAAT1, EAAT2, GFAP and β-actin. (B) Densitometric analysis showing the expression levels of the EAATs or GFAP normalized to β-actin. Data are presented as the mean ± standard deviation (n=6). **P<0.01 compared with the control group (prior to TNF-α treatment, 0 h). TNF-α, tumor necrosis factor-α; EAAT, excitatory amino-acid transporter; GFAP, glial fibrillary acidic protein.
Mentions: To further explore the association between incubation time and the expression levels of EAATs in astrocytes, the astrocytes were treated with the optimal concentration of TNF-α (10 ng/ml) for different incubation periods (4, 8, 12, 24, 36 or 72 h). The EAAT2 protein expression showed a time-dependent increase, followed by a time-dependent decrease, with a maximum level (P<0.01) after 12 h (Fig. 3). However, the expression levels of EAAT1 and GFAP did not change with treatment. These results indicated that short-term treatment with the optimal concentration of TNF-α promoted EAAT2 expression in astrocytes, which was independent of astrocyte proliferation.

Bottom Line: The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia.The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change.The present results suggest that a relatively short-term application of an optimal concentration of TNF-α may protect neurons against ischemic injury by elevating the expression of EAAT2 in astrocytes.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Zhejiang University City College, Hangzhou, Zhejiang 310015, P.R. China ; Department of Basic Medicine, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.

ABSTRACT
The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia. Exogenous TNF-α was administered to pure cultured astrocytes and the expression levels of EAAT1, EAAT2 and glial fibrillary acidic protein (GFAP) were evaluated. The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change. To determine whether the elevation in the levels of the EAAT2 protein induced by TNF-α had a beneficial effect on ischemic insult, TNF-α was applied to in vitro models of cerebral ischemia; the treatment was observed to increase neuronal viability. The present results suggest that a relatively short-term application of an optimal concentration of TNF-α may protect neurons against ischemic injury by elevating the expression of EAAT2 in astrocytes.

No MeSH data available.


Related in: MedlinePlus