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Metformin Prevents H?O?-Induced Senescence in Human Lens Epithelial B3 Cells.

ABSTRACT: BACKGROUND The primary purpose of this study was to investigate the protective effect of metformin against hydrogen peroxide (H?O?)-induced cellular senescence and to explore the underlying molecular mechanism of lens epithelial cell senescence. MATERIAL AND METHODS We used H?O? to establish senescence in human lens epithelial B3 cells. The cells were exposed to H?O? for different numbers of days to mimic aging. Senescence was assessed by senescence-associated ß-galactosidase staining, and the molecular mechanism was assessed by real-time polymerase chain reaction (RT-PCR) and western blot analysis. The cultured cells were exposed to 150 ?M H?O? for 7 days with or without metformin to detect the underlying molecular mechanism of lens epithelial cell senescence. RESULTS The lens epithelial cells exposed to 150 µM H?O? for 7 days exhibited senescence. The expression levels of senescence-related markers were increased in H?O?-treated cells. Metformin prevented H?O?-induced cellular senescence in human lens epithelial B3 cells. CONCLUSIONS These findings suggest that senescence marker expression is increased in the cells exposed to H?O?. Metformin protects human lens epithelial B3 cells from H?O?-induced senescence.

SUBMITTER: Zhang C

PROVIDER: S-EPMC7202252 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Metformin Prevents H₂O₂-Induced Senescence in Human Lens Epithelial B3 Cells.

Zhang Chunmei C Chen Mengmeng M Zhou Nan N Qi Yanhua Y

Medical science monitor basic research 20200427

BACKGROUND The primary purpose of this study was to investigate the protective effect of metformin against hydrogen peroxide (H₂O₂)-induced cellular senescence and to explore the underlying molecular mechanism of lens epithelial cell senescence. MATERIAL AND METHODS We used H₂O₂ to establish senescence in human lens epithelial B3 cells. The cells were exposed to H₂O₂ for different numbers of days to mimic aging. Senescence was assessed by senescence-associated ß-galactosidase staining, and the m ...[more]

PMID: 32336745

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Project description:Connexin (Cx) proteins form gap junction channels (GJC) and hemichannels that a allow bidirectional flow of ions and metabolites between the cytoplasm and extracellular space, respectively. Under physiological conditions, hemichannels have a very low probability of opening, but in certain pathologies, hemichannels activity can increase and induce and/or accelerate cell death. Several mechanisms control hemichannels activity, including phosphorylation and oxidation (i.e., S-nitrosylation). Recently, the effect of polyunsaturated fatty acids (PUFAs) such as linoleic acid (LA), were found to modulate Cxs. It has been seen that LA increase cell death in bovine and human lens cells. The lens is a structure allocated in the eye that highly depends on Cx for the metabolic coupling between its cells, a condition necessary for its transparency. Therefore, we hypothesized that LA induces lens cells death by modulating hemichannel activity. In this work, we characterized the effect of LA on hemichannel activity and survival of HLE-B3 cells (a human lens epithelial cell line). We found that HLE-B3 cells expresses Cx43, Cx46, and Cx50 and can form functional hemichannels in their plasma membrane. The extracellular exposure to 10-50 μM of LA increases hemichannels activity (dye uptake) in a concentration-dependent manner, which was reduced by Cx-channel blockers, such as the Cx-mimetic peptide Gap27 and TATGap19, La3+, carbenoxolone (CBX) and the Akt kinase inhibitor. Additionally, LA increases intracellular calcium, which is attenuated in the presence of TATGap19, a specific Cx43-hemichannel inhibitor. Finally, the long exposure of HLE-B3 cells to LA 20 and 50 μM, reduced cell viability, which was prevented by CBX. Moreover, LA increased the proportion of apoptotic HLE-B3 cells, effect that was prevented by the Cx-mimetic peptide TAT-Gap19 but not by Akt inhibitor. Altogether, these findings strongly suggest a contribution of hemichannels opening in the cell death induced by LA in HLE-B3 cells. These cells can be an excellent tool to develop pharmacological studies in vitro.

Dataset Information

Metformin Prevents H?O?-Induced Senescence in Human Lens Epithelial B3 Cells.

Publications

Metformin Prevents H₂O₂-Induced Senescence in Human Lens Epithelial B3 Cells.

Similar Datasets

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