Mitochondrial Dysfunctions Suppress the NGF- Regulated Neurite Elongation and Apoptosis in PC12 Cells
Date Issued
2006
Date
2006
Author(s)
Ji, Hong-Tai
DOI
zh-TW
Abstract
In cells, mitochondria are the major ATP source produced by oxidative phosphorylation. In addition, mitochondria are critical for other aspects of cell function, such as modulating calcium levels. Consequently, mitochondrial dysfunction contributes to a wide range of human diseases, including neurodegenerative diseases. Neurons are highly dependent on oxidative energy metabolism, therefore normal mitochondrial function is the key pathogenic factor in a number of neurodegenerative disorders. In our study, using 5- aminolevulinic acid mediated photodynamic treatment（ALA-PDT）, PC12 variants with dysfunctional mitochondria were established. The purpose of this study is to address the post-PDT responses in PC12 cells survived from mitochondrial photodamage induced by ALA-PDT.
We found：（1）ALA-PDT could be used to establish enlarged PC12 variants with dysfunctional mitochondria.（2）In the presence of NGF, morphology was changed and neurite elongation was suppressed in differentiated PC12 variants with dysfunctional mitochondria.（3）In the absence of NGF, apoptotic cell death was suppressed in PC12 variants with dysfunctional mitochondria in serum-free or low-serum medium.（4）Activated ERK decreased in PC12 variants with dysfunctional mitochondria, but JNK not.（5）In mRNA microarray analysis, expression of calcium- and neuro- related gene decreased in PC12 variants with dysfunctional mitochondria.
Subjects
粒腺體功能異常
PC12 細胞
mitochondrial dysfunction
PC12 cell
SDGs
Type
other
File(s)![Thumbnail Image]()
Loading...
Name
ntu-95-R92450015-1.pdf
Size
23.31 KB
Format
Adobe PDF
Checksum
(MD5):06b7cc9496e2ee68fcdfacb8a35a0fe1