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Upregulation of adenosine kinase in Rasmussen encephalitis.

Luan G, Gao Q, Guan Y, Zhai F, Zhou J, Liu C, Chen Y, Yao K, Qi X, Li T - J. Neuropathol. Exp. Neurol. (2013)

Bottom Line: Immunohistochemistry was used to examine the expression of ADK and glial fibrillary acidic protein in surgically resected human epileptic cortical specimens from RE patients (n = 12) and compared with control cortical tissues (n = 6).Focal astrogliosis and marked expression of ADK were observed in the lesions of RE.These results suggest that upregulation of ADK is a common pathologic hallmark of RE and that ADK might be a target in the treatment of epilepsy associated with RE.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery (GL, YG, FZ, JZ, CL), Brain Institute (QG, YC, TL), and Department of Neurology (TL), Epilepsy Center, and Department of Neuropathology (KY, XQ), Beijing Sanbo Brain Hospital, Capital Medical University, Beijing, China.

ABSTRACT
Rasmussen encephalitis (RE) is a rare neurologic disorder of childhood characterized by unihemispheric inflammation, progressive neurologic deficits, and intractable focal epilepsy. The pathogenesis of RE is still enigmatic. Adenosine is a key endogenous signaling molecule with anticonvulsive and anti-inflammatory effects, and our previous work demonstrated that dysfunction of the adenosine kinase (ADK)-adenosine system and astrogliosis are the hallmarks of epilepsy. We hypothesized that the epileptogenic mechanisms underlying RE are related to changes in ADK expression and that those changes might be associated with the development of epilepsy in RE patients. Immunohistochemistry was used to examine the expression of ADK and glial fibrillary acidic protein in surgically resected human epileptic cortical specimens from RE patients (n = 12) and compared with control cortical tissues (n = 6). Adenosine kinase expression using Western blot and enzymatic activity for ADK were assessed in RE versus control samples. Focal astrogliosis and marked expression of ADK were observed in the lesions of RE. Significantly greater ADK expression in RE versus controls was demonstrated by Western blot, and greater enzymatic activity for ADK was demonstrated using an enzyme-coupled bioluminescent assay. These results suggest that upregulation of ADK is a common pathologic hallmark of RE and that ADK might be a target in the treatment of epilepsy associated with RE.

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Western blot analysis of adenosine kinase (ADK) in RE and control specimens. (A) Representative immunoblots of ADK (∼40 kDa) in total homogenates of RE and control specimens. Beta-actin immunoreactivity was used to normalize for equal protein loading. (B) Quantitative analysis of ADK expression levels. Data are mean ± SEM (n = 3 per group). * p < 0.05 vs control.
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Figure 5: Western blot analysis of adenosine kinase (ADK) in RE and control specimens. (A) Representative immunoblots of ADK (∼40 kDa) in total homogenates of RE and control specimens. Beta-actin immunoreactivity was used to normalize for equal protein loading. (B) Quantitative analysis of ADK expression levels. Data are mean ± SEM (n = 3 per group). * p < 0.05 vs control.

Mentions: Western blot analysis was also performed to quantify the total amount of ADK in total homogenates of control autopsy cortex and surgical cortex from RE patients (Fig. 5A). There was significantly greater ADK expression (p < 0.05) in RE versus control specimens (Fig. 5B).


Upregulation of adenosine kinase in Rasmussen encephalitis.

Luan G, Gao Q, Guan Y, Zhai F, Zhou J, Liu C, Chen Y, Yao K, Qi X, Li T - J. Neuropathol. Exp. Neurol. (2013)

Western blot analysis of adenosine kinase (ADK) in RE and control specimens. (A) Representative immunoblots of ADK (∼40 kDa) in total homogenates of RE and control specimens. Beta-actin immunoreactivity was used to normalize for equal protein loading. (B) Quantitative analysis of ADK expression levels. Data are mean ± SEM (n = 3 per group). * p < 0.05 vs control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3815008&req=5

Figure 5: Western blot analysis of adenosine kinase (ADK) in RE and control specimens. (A) Representative immunoblots of ADK (∼40 kDa) in total homogenates of RE and control specimens. Beta-actin immunoreactivity was used to normalize for equal protein loading. (B) Quantitative analysis of ADK expression levels. Data are mean ± SEM (n = 3 per group). * p < 0.05 vs control.
Mentions: Western blot analysis was also performed to quantify the total amount of ADK in total homogenates of control autopsy cortex and surgical cortex from RE patients (Fig. 5A). There was significantly greater ADK expression (p < 0.05) in RE versus control specimens (Fig. 5B).

Bottom Line: Immunohistochemistry was used to examine the expression of ADK and glial fibrillary acidic protein in surgically resected human epileptic cortical specimens from RE patients (n = 12) and compared with control cortical tissues (n = 6).Focal astrogliosis and marked expression of ADK were observed in the lesions of RE.These results suggest that upregulation of ADK is a common pathologic hallmark of RE and that ADK might be a target in the treatment of epilepsy associated with RE.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery (GL, YG, FZ, JZ, CL), Brain Institute (QG, YC, TL), and Department of Neurology (TL), Epilepsy Center, and Department of Neuropathology (KY, XQ), Beijing Sanbo Brain Hospital, Capital Medical University, Beijing, China.

ABSTRACT
Rasmussen encephalitis (RE) is a rare neurologic disorder of childhood characterized by unihemispheric inflammation, progressive neurologic deficits, and intractable focal epilepsy. The pathogenesis of RE is still enigmatic. Adenosine is a key endogenous signaling molecule with anticonvulsive and anti-inflammatory effects, and our previous work demonstrated that dysfunction of the adenosine kinase (ADK)-adenosine system and astrogliosis are the hallmarks of epilepsy. We hypothesized that the epileptogenic mechanisms underlying RE are related to changes in ADK expression and that those changes might be associated with the development of epilepsy in RE patients. Immunohistochemistry was used to examine the expression of ADK and glial fibrillary acidic protein in surgically resected human epileptic cortical specimens from RE patients (n = 12) and compared with control cortical tissues (n = 6). Adenosine kinase expression using Western blot and enzymatic activity for ADK were assessed in RE versus control samples. Focal astrogliosis and marked expression of ADK were observed in the lesions of RE. Significantly greater ADK expression in RE versus controls was demonstrated by Western blot, and greater enzymatic activity for ADK was demonstrated using an enzyme-coupled bioluminescent assay. These results suggest that upregulation of ADK is a common pathologic hallmark of RE and that ADK might be a target in the treatment of epilepsy associated with RE.

Show MeSH
Related in: MedlinePlus