Inhibition of VDAC1 prevents Ca2+-mediated oxidative stress and apoptosis induced by 5-aminolevulinic acid mediated sonodynamic therapy in THP-1 macrophages
详细信息 查看全文
- 作者：Haibo Chen (1)
Weiwei Gao (2)
Yang Yang (1)
Shuyuan Guo (1)
Huan Wang (1)
Wei Wang (1)
Shuisheng Zhang (3)
Qi Zhou (4)
Haobo Xu (1)
Jianting Yao (1)
Zhen Tian (2)
Bicheng Li (1)
Wenwu Cao (5)
Zhiguo Zhang (4)
Ye Tian (1) (2) - 关键词：Sonodynamic therapy ; Macrophage ; Apoptosis ; Voltage ; dependent anion channel 1 ; Reactive oxygen species ; Calcium
- 刊名：Apoptosis
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：19
- 期：12
- 页码：1712-1726
- 全文大小：4,607 KB
- 参考文献：1. Yumita N, Nishigaki R, Umemura K, Umemura S (1989) Hematoporphyrin as a sensitizer of cell-damaging effect of ultrasound. Jpn J Cancer Res 80:219-22 CrossRef
2. Trendowski M (2013) The promise of sonodynamic therapy. Cancer Metastasis Rev. doi:10.1007/s10555-013-9461-5
3. Gao Q, Wang F, Guo S, Li J, Zhu B, Cheng J, Jin Y, Li B, Wang H, Shi S, Zhang Z, Cao W, Tian Y (2011) Sonodynamic effect of an anti-inflammatory agent–emodin on macrophages. Ultrasound Med Biol 37:1478-485 CrossRef
4. Guo S, Sun X, Cheng J, Xu H, Dan J, Shen J, Zhou Q, Zhang Y, Meng L, Cao W, Tian Y (2013) Apoptosis of THP-1 macrophages induced by protoporphyrin IX-mediated sonodynamic therapy. Int J Nanomed 8:2239-246
5. Zheng L, Sun X, Zhu X, Lv F, Zhong Z, Zhang F, Guo W, Cao W, Yang L, Tian Y (2014) Apoptosis of THP-1 derived macrophages induced by sonodynamic therapy using a new sonosensitizer hydroxyl acetylated curcumin. PLoS ONE 9:e93133 CrossRef
6. Moore KJ, Sheedy FJ, Fisher EA (2013) Macrophages in atherosclerosis: a dynamic balance. Nat Rev Immunol 13:709-21 CrossRef
7. Libby P, Lichtman AH, Hansson GK (2013) Immune effector mechanisms implicated in atherosclerosis: from mice to humans. Immunity 38:1092-104 CrossRef
8. Weber C, Noels H (2011) Atherosclerosis: current pathogenesis and therapeutic options. Nat Med 17:1410-422 CrossRef
9. De Meyer I, Martinet W, De Meyer GR (2012) Therapeutic strategies to deplete macrophages in atherosclerotic plaques. Br J Clin Pharmacol 74:246-63 CrossRef
10. Peng C, Li Y, Liang H, Cheng J, Li Q, Sun X, Li Z, Wang F, Guo Y, Tian Z, Yang L, Tian Y, Zhang Z, Cao W (2011) Detection and photodynamic therapy of inflamed atherosclerotic plaques in the carotid artery of rabbits. J Photochem Photobiol, B 102:26-1 CrossRef
11. Nielsen KP, Juzeniene A, Juzenas P, Stamnes K, Stamnes JJ, Moan J (2005) Choice of optimal wavelength for PDT: the significance of oxygen depletion. Photochem Photobiol 81:1190-194 CrossRef
12. Cheng J, Sun X, Guo S, Cao W, Chen H, Jin Y, Li B, Li Q, Wang H, Wang Z, Zhou Q, Wang P, Zhang Z, Tian Y (2013) Effects of 5-aminolevulinic acid-mediated sonodynamic therapy on macrophages. Int J Nanomed 8:669-76 CrossRef
13. Wang H, Yang Y, Chen H, Dan J, Cheng J, Guo S, Sun X, Wang W, Ai Y, Li S, Li Z, Peng L, Tian Z, Yang L, Wu J, Zhong X, Zhou Q, Wang P, Zhang Z, Cao W, Tian Y (2014) 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. Cell Physiol Biochem 33:1789-801 CrossRef
14. Shoshan-Barmatz V, De Pinto V, Zweckstetter M, Raviv Z, Keinan N, Arbel N (2010) VDAC, a multi-functional mitochondrial protein regulating cell life and death. Mol Aspects Med 31:227-85 CrossRef
15. Shoshan-Barmatz V, Israelson A, Brdiczka D, Sheu SS (2006) The voltage-dependent anion channel (VDAC): function in intracellular signalling, cell life and cell death. Curr Pharm Des 12:2249-270 CrossRef
16. Saks V, Guzun R, Timohhina N, Tepp K, Varikmaa M, Monge C, Beraud N, Kaambre T, Kuznetsov A, Kadaja L, Eimre M, Seppet E (2010) Structure-function relationships in feedback regulation of energy fluxes in vivo in health and disease: mitochondrial inter - 作者单位：Haibo Chen (1)
Weiwei Gao (2)
Yang Yang (1)
Shuyuan Guo (1)
Huan Wang (1)
Wei Wang (1)
Shuisheng Zhang (3)
Qi Zhou (4)
Haobo Xu (1)
Jianting Yao (1)
Zhen Tian (2)
Bicheng Li (1)
Wenwu Cao (5)
Zhiguo Zhang (4)
Ye Tian (1) (2)
1. Department of Cardiology, The First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, 23 Youzheng Street, Harbin, 150001, Heilongjiang, China
2. Department of Pathophysiology, The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin Medical University, Harbin, 150081, Heilongjiang, China
3. Department of Interventional Radiology and Vascular Surgery, Peking University First Hospital, Xi Shi Ku Street No. 8, Xi Cheng District, Beijing, 100034, China
4. Laboratory of Photo- and Sono-theranostic Technologies and Condensed Matter Science and Technology Institute, Harbin Institute of Technology, Harbin, 150081, Heilongjiang, China
5. Materials Research Institute, The Pennsylvania State University, University Park, PA, 16802, USA - ISSN：1573-675X
文摘
Ultrasound combined with endogenous protoporphyrin IX derived from 5-aminolevulinic acid (ALA-SDT) is known to induce apoptosis in multiple cancer cells and macrophages. Persistent retention of macrophages in the plaque has been implicated in the pathophysiology and progression of atherosclerosis. Here we investigated the effects of inhibition of voltage-dependent anion channel 1 (VDAC1) on ALA-SDT-induced THP-1 macrophages apoptosis. Cells were pre-treated with VDAC1 inhibitor 4,4-diisothiocyanostilbene-2,2-disulfonic acid (DIDS) disodium salt for 1?h or downregulated VDAC1 expression by small interfering RNA and exposed to ultrasound. Cell viability was assessed by MTT assay, and cell apoptosis along with necrosis was evaluated by Hoechst 33342/propidium iodide staining and flow cytometry. Levels of cytochrome c release was assessed by confocal microscope and Western blot. The levels of full length caspases, caspase activation, and VDAC isoforms were analyzed by Western blot. Intracellular reactive oxygen species generation, mitochondrial membrane permeability, and intracellular Ca2+ [Ca2+]i levels were measured with fluorescent probes. We confirmed that the pharmacological inhibition of VDAC1 by DIDS notably prevented ALA-SDT-induced cell apoptosis in THP-1 macrophages. Additionally, DIDS significantly inhibited intracellular ROS generation and apoptotic biochemical changes such as inner mitochondrial membrane permeabilization, loss of mitochondrial membrane potential, cytochrome c release and activation of caspase-3 and caspase-9. Moreover, ALA-SDT elevated the [Ca2+]i levels and it was also notably reduced by DIDS. Furthermore, both of intracellular ROS generation and cell apoptosis were predominately inhibited by Ca2+ chelating reagent BAPTA-AM. Intriguingly, ALA-treatment markedly augmented VDAC1 protein levels exclusively, and the downregulation of VDAC1 expression by specific siRNA also significantly abolished cell apoptosis. Altogether, these results suggest that VDAC1 plays a crucial role in ALA-SDT-induced THP-1 macrophages apoptosis, and targeting VDAC1 is a potential way regulating macrophages apoptosis, a finding that may be relevant to therapeutic strategies against atherosclerosis.