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The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
| Content Provider | Semantic Scholar |
|---|---|
| Author | Wang, Huan Yang, Yang Chen, Haibo Dan, Juhua Cheng, Jiali Guo, Shuyuan Wang, Wei Ai, Yiwei Li, Shuchang Li, Zhixin Peng, Li Tian, Zhen Yuan Yang, Liming Wu, Jichao Zhong, Xin Zhou, Qi Wang, Peng Zhang, Zhiguo Cao, Wenwu Tian, Ye |
| Copyright Year | 2014 |
| Abstract | Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. |
| Starting Page | 1789 |
| Ending Page | 1801 |
| Page Count | 13 |
| File Format | PDF HTM / HTML |
| DOI | 10.1159/000362958 |
| PubMed reference number | 24923653 |
| Journal | Medline |
| Volume Number | 33 |
| Alternate Webpage(s) | https://www.karger.com/Article/Pdf/362958 |
| Alternate Webpage(s) | https://doi.org/10.1159/000362958 |
| Journal | Cellular Physiology and Biochemistry |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |