Involvement of Caspases and Bcl-2 Family in Nitric Oxide-Induced Apoptosis of Rat PC12 Cells.
- Author:
Yeon Jin JEONG
1
;
Ji Yeon JUNG
;
Jin Ha LEE
;
Jin Hyoung CHO
;
Guem Sug LEE
;
Sun Hun KIM
;
Won Jae KIM
Author Information
1. Dental Science Research Institute, 2nd Stage of Brain Korea 21, School of Dentistry, Chonnam National University, Gwangju, Korea. jjy@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Nitric oxide;
PC12 cells;
Bcl-2 family;
Caspase
- MeSH:
Animals;
Apoptosis*;
Caspases*;
Chromatin;
Cytochromes c;
Cytosol;
DNA Fragmentation;
Humans;
Mitochondria;
Nitric Oxide;
Nitroprusside;
PC12 Cells*;
Rats*;
Reactive Oxygen Species;
Tissue Donors
- From:The Korean Journal of Physiology and Pharmacology
2006;10(6):329-335
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study was aimed to investigate the nitric oxide (NO)-induced cytotoxic mechanism in PC12 cells. Sodium nitroprusside (SNP), an NO donor, decreased the viability of PC12 cells in dose- and time-dependent manners. SNP enhanced the production of reactive oxygen species (ROS), and gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. Expression of Bax was not affected, whereas Bcl-2 was downregulated in SNP-treated PC12 cells. SNP augmented the release of cytochrome c from mitochondria into cytosol and enhanced caspase -8, -9, and -3 activities. SNP upregulated both Fas and Fas-L, which are known to be components of death receptor assembly. These results suggest that NO induces apoptosis of PC12 cells through both mitochondria- and death receptor-mediated pathways mediated by ROS and Bcl-2 family.
