Basic FGF attenuates amyloid β-peptide-induced oxidative stress, mitochondrial dysfunction, and impairment of Na+/K+-ATPase activity in hippocampal neurons
Abstract
Basic fibroblast growth factor (bFGF) exhibits trophic activity for many populations of neurons in the brain, and can protect those neurons against excitotoxic, metabolic and oxidative insults. In Alzheimer's disease (AD), amyloid beta-peptide (A beta) fibrils accumulate in plaques which are associated with degenerating neurons. A beta can be neurotoxic by a mechanism that appears to involve induction of oxidative stress and disruption of calcium homeostasis. Plaques in AD brain contain high levels of bFGF suggesting a possible modulatory role for bFGF in the neurodegenerative process. We now report that bFGF can protect cultured hippocampal neurons against A beta25-35 toxicity by a mechanism that involves suppression of reactive oxygen species (ROS) accumulation and maintenance of Na+/K+-ATPase activity. A beta25-35 induced lipid peroxidation, accumulation of H2O2, mitochondrial ROS accumulation, and a decrease in mitochondrial transmembrane potential; each of these effects of A beta25-35 was abrogated in cultures pre-treated with bFGF. Na+/K+-ATPase activity was significantly reduced following exposure to A beta25-35 in control cultures, but not in cultures pre-treated with bFGF. bFGF did not protect neurons from death induced by ouabain (a specific inhibitor of the Na+/K+-ATPase) or 4-hydroxynonenal (an aldehydic product of lipid peroxidation) consistent with a site of action of bFGF prior to induction of oxidative stress and impairment of ion-motive ATPases. By suppressin…
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FGF2 protects neurons against conditions associated with inflammation including oxidative stress and excitotoxicity.
“FGF2 is also known to protect neurons against conditions associated with inflammation including oxidative stress and excitotoxicity (Mattson et al., 1989; Mark et al., 1997), suggesting that suppression of FGF2 production by miR-181s could render neurons vulnerable to such adverse conditions.”
From Evidence for miR‐181 involvement in neuroinflammatory responses of astrocytes (2013) · cites this paper as Mark et al., 1997
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- Authors
- Mark, R. J., Keller, J. N., Kruman, I., & Mattson, M. P.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 1997-05
- Volume
- 756
- Issue
- 1-2
- Pages
- 205-214
- ISSN
- 0006-8993
- Cited by
- 141
- References
- 4
- Language
- en
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