Abstract
Exposure of mammalian cells to ultraviolet (UV) light elicits a cellular response and also lead to apoptotic cell death. However, the role of Rac, a member of Rho family GTPases, in the UV-induced apoptosis has never been examined. In UV-irradiated Rat-2 fibroblasts, nuclear fragmentation began to be observed within 2 h and the total viability of Rat-2 cells were only about 15% at 6 h following by UV irradiation, whereas the total viability in Rat2-RacN17 cells stably expressing RacN17, a dominant negative Rac1 mutant, was almost close to 67%. Pretreatment with SB203580, a specific inhibitor of p38 kinase, likewise attenuated UV-induced cell death, but PD98059, a MEK inhibitor, did not. Thus, Rac1 and p38 kinase appear to be components in the apoptotic signaling pathway induced by UV irradiation in Rat-2 fibroblasts. In addition, our results show that p38 kinase stimulation by UV is dramatically inhibited by RacN17, suggesting that p38 kinase is situated downstream of Rac1 in the UV signaling to apoptosis.
| Original language | English |
|---|---|
| Pages (from-to) | 825-829 |
| Number of pages | 5 |
| Journal | Biochemical and biophysical research communications |
| Volume | 285 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2001 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by grants from the National Research Laboratory (NRL), Life Phenomena and Function Research Group Program-2000 from the Ministry of Science and Technology, and the Brain Korea 21 (BK21) program.
Keywords
- Apoptosis
- Rac
- UV
- p38 kinase
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology