Related Experiment Videos
Fibroblast growth factor induces beta-amyloid precursor mRNA in glial but not neuronal cultured cells
D Quon1, R Catalano, B Cordell
1California Biotechnology, Inc., Mountain View 94043.
Abstract:
Treatment of PC12 and C6 cell cultures with recombinant basic fibroblast growth factor results in approximately a five to ten-fold stimulation of beta-amyloid precursor mRNA in the C6 astrocytoma cell line but only a slight induction of precursor mRNA in the PC-12 neuronal cell line. Stimulation of expression occurred at a hormone concentration of approximately 0.5 to 1 nM and was seen after 2 days. These results suggest that basic fibroblast growth factor may contribute to amyloidosis of Alzheimer's disease.
Insights
Basic fibroblast growth factor significantly increases beta-amyloid precursor mRNA in C6 astrocytoma cells, but not PC-12 neuronal cells. This suggests a potential role for this growth factor in Alzheimer
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Alzheimer's disease is characterized by amyloid plaques.
- The role of growth factors in neurodegenerative diseases is under investigation.
Purpose of the Study:
- To investigate the effect of basic fibroblast growth factor (bFGF) on beta-amyloid precursor mRNA expression in neuronal and astrocytoma cell lines.
- To explore the potential link between bFGF and amyloidosis.
Main Methods:
- Treatment of PC12 (neuronal) and C6 (astrocytoma) cell cultures with recombinant bFGF.
- Quantification of beta-amyloid precursor mRNA levels via RT-PCR.
- Dose-response and time-course analysis of bFGF stimulation.
Main Results:
- bFGF treatment resulted in a 5-10 fold increase in beta-amyloid precursor mRNA in C6 cells.
- PC12 cells showed only a slight induction of precursor mRNA following bFGF treatment.
- Stimulation was observed at 0.5-1 nM bFGF and after 2 days.
Conclusions:
- Basic fibroblast growth factor differentially affects beta-amyloid precursor expression in neuronal and astrocytoma cells.
- These findings suggest a potential contribution of bFGF to the development of amyloidosis in Alzheimer's disease.