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Programmed cell death of PC12 induced by adenovirus E1A
M Sawada1, N Kondo, T Marunouchi
1Division of Cell Biology, Fujita Health University, Aichi, Japan.
Neuroscience Letters
|May 26, 1995
Summary
Scientists developed a serum-deprived resistant PC12 cell subclone, PC12FrR, which showed altered growth. Adenovirus E1A gene transfection in PC12FrR cells restored serum-deprived cell death, suggesting E1A
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- PC12 rat pheochromocytoma cells normally undergo apoptosis with DNA fragmentation when deprived of serum.
- A subclone, PC12FrR, was isolated exhibiting resistance to this serum-deprived apoptosis.
Purpose of the Study:
- To investigate the role of Adenovirus E1A gene products in regulating neuronal cell growth and death.
- To understand the mechanisms underlying serum deprivation-induced apoptosis in PC12 cells.
Main Methods:
- Isolation of a serum-deprived apoptosis-resistant PC12 subclone (PC12FrR).
- Characterization of PC12FrR cell growth and size compared to parental PC12 cells.
- Transfection of PC12FrR cells with the Adenovirus E1A gene and assessment of cell growth and apoptosis under serum-rich and serum-deprived conditions.
Main Results:
- PC12FrR cells exhibited slightly faster growth and larger cell size than parental PC12 cells.
- Adenovirus E1A gene-transfected PC12FrR cells demonstrated significantly accelerated growth in the presence of serum.
- In serum-deprived conditions, E1A-transfected PC12FrR cells underwent apoptosis with DNA fragmentation, similar to parental PC12 cells.
Conclusions:
- The Adenovirus E1A gene product appears to play a role in overcoming resistance to serum deprivation-induced apoptosis.
- E1A gene targets may be critical components of the regulatory mechanisms governing neuronal cell growth and programmed cell death.
- This study provides insights into the molecular pathways controlling neuronal cell fate.