Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0043320100330020285
Archives of Pharmacal Research
2010 Volume.33 No. 2 p.285 ~ p.291
Interferon-¥ã Enhances the Apoptosis of Macrophages Under Trophic Stress through Activation of p53 and the JAK1 Pathway
Pyo Suhk-Neung

Cho Seong-Jun
Abstract
Apoptosis has been implicated as an important mediator of immunosuppression associated with a depleted nutritional state. Since a number of cytokines are likely to influence the rate of apoptosis, we determined the effect of interferon-gamma (IFN-¥ã) on apoptosis of macrophages in serum/amino acid deprived cell culture conditions. IFN-¥ã further increased the rate of apoptosis compared to trophically stressed macrophages. In addition, we showed that enhancement of apoptosis by IFN-¥ã is caused by a decrease in mitochondrial membrane potential due to upregulation of p53 and Bax and down-regulation of Bcl-xL. Moreover, we found that IFN-¥ã increases caspase-3 activity that had been induced by serum/amino acid depletion, and that JAK1 signaling is involved in capase-3 activation and in the enhancement of apoptosis by IFN-¥ã.
KEYWORD
IFN-¥ã, Apoptosis, p53, JAK1, Macrophages
FullTexts / Linksout information
Listed journal information
SCI(E) MEDLINE ÇмúÁøÈïÀç´Ü(KCI)