Cyclic amp-induced differentiation increases the synthesis of extracellular superoxide dismutase in rat c6 glioma
Autor: | Herman Slegers, Jean Willems, An Zwijsen, Els Van Mechelen, Stefan Nicolai |
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Rok vydání: | 1996 |
Předmět: |
Transcription
Genetic Cell 8-Bromo Cyclic Adenosine Monophosphate Stimulation Biology Biochemistry Isozyme Cell Line Transcription (biology) Physiology (medical) Glial Fibrillary Acidic Protein Cyclic AMP medicine Transcriptional regulation Animals RNA Messenger Enzyme Inhibitors Protein kinase A Sulfonamides Messenger RNA Superoxide Dismutase Cell Differentiation Glioma Isoquinolines Cyclic AMP-Dependent Protein Kinases Molecular biology Rats Cell biology Kinetics medicine.anatomical_structure Bucladesine Extracellular Space Transforming growth factor |
Zdroj: | Free radical biology and medicine |
ISSN: | 0891-5849 |
DOI: | 10.1016/0891-5849(96)00122-0 |
Popis: | The effect of membrane permeable cAMP analogues on the expression of extracellular superoxide dismutase (EC-SOD) was studied in rat C6 glioma. EC-SOD is constitutively expressed but stimulation with cAMP analogues still increased the EC-SOD transcription and the secreted SOD activity. The potency to enhance EC-SOD expression is correlated with the ability of the cAMP analogue to induce cAMP-dependent differentiation in C6. The increase in EC-SOD mRNA and in secreted activity depended on the concentration of the cAMP analogues and on the cultivation time. Twenty-four hours after addition of 0.5 mM N6, O'2-dibutyryl cAMP (dbcAMP) or N6-monobutyryl cAMP (N6-mbcAMP) EC-SOD mRNA expression increased approximately twofold, while stimulation for 68 h with 0.5 mM N6-mbcAMP or 1 mM 8-Chloro cAMP (ClcAMP) and 1 mM dbcAMP enhanced the mean secreted activity/cell three- and fivefold, respectively. O'2-monobutyryl cAMP (O'2-mbcAMP) did not affect EC-SOD synthesis. The enhancement in EC-SOD activity did not require activation of protein kinase A. ATP, TGF-beta, IFN-gamma, and LPS did not affect EC-SOD synthesis. The presented data point to a cAMP-dependent pathway for the enhanced expression of EC-SOD by glial cells in brain. |
Databáze: | OpenAIRE |
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