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Published on: October 17, 2017
Mitochondrion-Targeted Peptide SS-31 Inhibited Oxidized Low-Density Lipoproteins-Induced Foam Cell Formation through
Shuangying Hao1, Jiajie Ji2, Hongting Zhao3
1Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University, Nanjing 210093, China. shuangying9088@163.com.
Abstract:
Foam cell formation as a result of imbalance of modified cholesterol influx and efflux by macrophages is a key to the occurrence and development of atherosclerosis. Oxidative stress is thought to be involved in the pathogenesis of atherosclerosis. SS-31 is a member of the Szeto-Schiller (SS) peptides shown to specifically target the inner mitochondrial membrane to scavenge reactive oxygen species. In this study, we investigated whether SS-31 may provide protective effect on macrophage from foam cell formation in RAW264.7 cells. The results showed that SS-31 inhibited oxidized low-density lipoproteins (ox-LDL)-induced foam cell formation and cholesterol accumulation, demonstrated by intracellular oil red O staining and measurement of cholesterol content. The mechanism was revealed that SS-31 did not only significantly attenuated ox-LDL-induced generation of reactive oxygen species (ROS) and increased the activities of superoxide dismutases, but also dose-dependently inhibited the expression of CD36 and LOX-1, two scavenger receptors of ox-LDL, while the expression of ATP-binding cassette A1 and G1, playing a pivotal role in cholesterol efflux, was not affected. As a result, SS-31 decreased pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha, suggesting the prevention of inflammatory responses. In conclusion, our results demonstrate that SS-31 provides a beneficial effect on macrophages from foam cell formation, likely, through both ROS scavenging and inhibition of cholesterol influx. Therefore, SS-31 may potentially be of therapeutic relevance in prevention of human atherogenesis.
Insights
SS-31 peptide prevents foam cell formation in macrophages by reducing cholesterol buildup and oxidative stress. This suggests SS-31 may be a potential therapeutic for preventing atherosclerosis.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Foam cell formation in macrophages, driven by cholesterol imbalance, is central to atherosclerosis.
- Oxidative stress is implicated in the pathogenesis of atherosclerosis.
- Szeto-Schiller (SS) peptides, like SS-31, target mitochondria to scavenge reactive oxygen species (ROS).
Purpose of the Study:
- To investigate the protective effects of SS-31 against foam cell formation in RAW264.7 macrophage cells.
- To elucidate the underlying mechanisms of SS-31's action on macrophage cholesterol metabolism and oxidative stress.
Main Methods:
- RAW264.7 cells were treated with oxidized low-density lipoproteins (ox-LDL) with or without SS-31.
- Foam cell formation was assessed via Oil Red O staining and cholesterol content measurement.
- ROS generation, superoxide dismutase activity, scavenger receptor (CD36, LOX-1) expression, and cholesterol efflux transporter (ABCA1, ABCG1) expression were analyzed.
Main Results:
- SS-31 significantly inhibited ox-LDL-induced foam cell formation and intracellular cholesterol accumulation.
- SS-31 attenuated ROS generation and enhanced superoxide dismutase activity.
- SS-31 dose-dependently reduced the expression of CD36 and LOX-1, without affecting ABCA1/ABCG1 expression.
- SS-31 decreased pro-inflammatory cytokines, including interleukin-6 and tumor necrosis factor-alpha.
Conclusions:
- SS-31 demonstrates a protective effect against macrophage foam cell formation.
- The mechanism involves ROS scavenging, inhibition of ox-LDL scavenger receptor expression, and subsequent reduction in cholesterol influx.
- SS-31 holds potential therapeutic relevance for preventing human atherogenesis.
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