Tat-DJ-1 enhances cell survival by inhibition of oxidative stress, NF-κB and MAPK activation in HepG2 cells
| Autor: | Min Jea Shin, Yeon Joo Choi, Su Bin Cho, Eun Ji Yeo, Hyo Sang Jo, Won Sik Eum, Chi Hern Lee, Jung Hwan Park, Soo Young Choi, Hyeon Ji Yeo |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Programmed cell death Cell Survival Recombinant Fusion Proteins p38 mitogen-activated protein kinases Apoptosis Bioengineering DNA Fragmentation medicine.disease_cause p38 Mitogen-Activated Protein Kinases Applied Microbiology and Biotechnology 03 medical and health sciences chemistry.chemical_compound Transduction Genetic medicine Humans bcl-2-Associated X Protein 030102 biochemistry & molecular biology JNK Mitogen-Activated Protein Kinases NF-kappa B Wild type NF-κB Hep G2 Cells Hydrogen Peroxide General Medicine Molecular biology Cell biology Oxidative Stress 030104 developmental biology Proto-Oncogene Proteins c-bcl-2 chemistry DNA fragmentation Reactive Oxygen Species Intracellular Oxidative stress Biotechnology |
| Zdroj: | Biotechnology Letters. 39:511-521 |
| ISSN: | 1573-6776 0141-5492 |
| DOI: | 10.1007/s10529-017-2286-5 |
| Popis: | To identify the protective effect of DJ-1 protein against oxidative stress-induced HepG2 cell death, we used cell-permeable wild type (WT) and a mutant (C106A Tat-DJ-1) protein. By using western blotting and fluorescence microscopy, we observed WT and C106A Tat-DJ-1 proteins were efficiently transduced into HepG2 cells. Transduced WT Tat-DJ-1 proteins increased cell survival and protected against DNA fragmentation and intracellular ROS generation levels in H2O2-exposed HepG2 cells. At the same time, transduced WT Tat-DJ-1 protein significantly inhibited NF-κB and MAPK (JNK and p38) activation as well as regulated the Bcl-2 and Bax expression levels. However, C106A Tat-DJ-1 protein did not show any protective effect against cell death responses in H2O2-exposed HepG2 cells. Oxidative stress-induced HepG2 cell death was significantly reduced by transduced WT Tat-DJ-1 protein, not by C106A Tat-DJ-1 protein. Thus, transduction of WT Tat-DJ-1 protein could be a novel strategy for promoting cell survival in situations of oxidative stress-induced HepG2 cell death. |
| Databáze: | OpenAIRE |
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