[Retracted] Mitochondrial‐Targeted Antioxidant Peptide SS31 Prevents RPE Cell Death under Oxidative Stress

Abstract

This work aims at investigating the protective effects of the mitochondria-targeted peptide SS31, on mitochondria function, preventing human retinal pigment epithelial cell-19 (ARPE-19) cell apoptosis. The ARPE-19 cells were subjected to 24 h of intervention with H2O2 of various concentrations (0, 100, 150, 200, 250, 300, and 500 μmol/L). Various concentrations of SS31 (10 nM, 100 nM, and 1 μmol/L) pretreated the cells for 2 h. The MTT assay determined cell viability. ARPE-19 cell apoptosis was observed by 4 ′ ,6-diamidino-2-phenylindole (DAPI) staining under fluorescence microscope and detected by Annexin-V/PI staining under flow cytometry. The measurement of reactive oxygen species (ROS) release level used MitoSOX Red (a mitochondrial superoxide indicator) and the probe 2 ′ -7 ′ dichlorofluorescin diacetate (DCFH-DA). And with the use of a JC-1 probe, the mitochondrial membrane potential (MMP; Δ Ψ m ) was analyzed. Reverse transcription polymerase chain reaction (RT-PCR) and real-time PCR were responsible for measuring the levels of apoptosis related genes (Bcl-2, Bax, and Caspase-3). The cell viability increased significantly with SS31 pretreated ( P < 0.05 ). In the SS 31 + H 2 O 2 group, the fluorescence of the cell nuclei with DAPI staining was weaker than H2O2 along group accordance with the decreased ratio of apoptotic cells ( P < 0.05 ). The ROS generation decreased in SS31 pretreated group, with the increased Δ Ψ m . The RT-PCR result showed decreased Bax gene and Caspase-3 gene expression with SS31 pretreatment, while increased antiapoptotic gene Bcl-2 ( P < 0.05 ). We provide evidence that SS31 promotes resilience of RPE cells to oxidative stress by stabilizing mitochondrial function.

Phloroglucinol Attenuates DNA Damage and Apoptosis Induced by Oxidative Stress in Human Retinal Pigment Epithelium ARPE-19 Cells by Blocking the Production of Mitochondrial ROS

“…Increased ROS in turn can inhibit mitochondrial efficiency, which can lead to more ROS production in mitochondria by a self-destructive vicious cycle [ 46 , 47 ]. Therefore, we evaluated whether ROS generated by H 2 O 2 was derived from mitochondria by applying MitoSOX-red, a mitochondrial superoxide indicator, and Mito-TEMPO, a specific antioxidant for mtROS based on previous studies showing that the generation of ROS induced by H 2 O 2 in ARPE-19 cells occurs in mitochondria [ 48 , 49 ]. MMP lost by H 2 O 2 was also significantly abolished by treatment with phloroglucinol or Mito-TEMPO alone.…”

Common methods in mitochondrial research (Review)

“…SS31 and mitoTEMPO are novel mitochondrial-targeted antioxidants that have a scavenging effect on ROS (443)(444)(445)(446). In addition, SS31 accumulates in the mitochondrial membrane to protect and restore the mitochondrial structure without affecting healthy mitochondria (162,(447)(448)(449)(450)(451)(452)(453). Thus, SS31 and mitoTEMPO have protective effects on a variety of diseases, including heart and kidney-related diseases, as well as sepsis and diabetes, which have been demonstrated in a variety of animal models (454)(455)(456)(457).…”

Retracted: Mitochondrial‐Targeted Antioxidant Peptide SS31 Prevents RPE Cell Death under Oxidative Stress

“…This article has been retracted by Hindawi, as publisher, following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of systematic manipulation of the publication and peer-review process.…”