Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 119, Issue -, Pages 171-177Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2017.10.017
Keywords
Astrocytes; Amyloid beta; Insulin; Reactive oxygen species
Categories
Funding
- JSPS KAKENHI [JP26850209, JP15J12259, JP 25450428, JP26450447, JP15K07768]
- Grants-in-Aid for Scientific Research [15K07768, 17H06880, 17K15390] Funding Source: KAKEN
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Insulin resistance in brain has been reported in Alzheimer's diseases (AD). Insulin signaling is important for homeostasis in brain function and reported to be disturbed in neurons leading to tau phosphorylation and neurofibrillary tangles. Many investigations of insulin in neurons have been reported; however, it has not been reported whether astrocytes also produce insulin. In the present study, we assessed the expression of insulin in astrocytes cultured from rat embryonic brain and the effects of amyloid beta(1-42) (A beta) and lipopolysaccharide (LPS) on the expression. We found that astrocytes expressed preproinsulin mRNAs and insulin protein, and that A beta or LPS decreased these expressions. Antioxidants, glutathione and N-acetylcysteine, restored the decreases in insulin mRNA expression by A beta and by LPS. Insulin protein was detected in astrocyte conditioned medium. These results suggest that astrocytes express and secrete insulin. Oxidative stress might be involved in the decreased insulin expression by A beta or LPS. The insulin decrease by A beta in astrocytes could be a novel disturbing mechanism for brain insulin signaling in AD. (C) 2017 Elsevier Ltd. All rights reserved.
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