4.1 Article

Role of glutathione and other antioxidants in the inhibition of apoptosis and mesenchymal transition in rabbit lens epithelial cells

Journal

GENETICS AND MOLECULAR RESEARCH
Volume 13, Issue 3, Pages 7149-7156

Publisher

FUNPEC-EDITORA
DOI: 10.4238/2014.September.1.1

Keywords

Lens epithelial cells; Glutathione; Catalase; Transforming growth factor beta 2; Mesenchymal transition; Reactive oxygen species

Funding

  1. National Natural Science Foundation of China [81270986]

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This study aimed to discuss the effect and mechanism of glutathione (GSH) and catalase (CAT) on transforming growth factor beta (TGF-beta)-induced lens epithelial cell (LEC) apoptosis and epithelial mesenchymal transition (EMT) to prevent and control cataracts. Healthy rabbits (4 weeks old) were randomly selected, and LECs from their lenses were cultured in vitro. The 2nd- and 3rd-generation cells were divided into 6 groups (group A: 75 pg/mL TGF-beta(2); B: 75 pg/mL TGF-beta(2) + 10 mM GSH; C: 75 pg/mL TGF-beta(2) + 300 U/mL CAT; D: 10 mM GSH; E: 300 U/mL CAT; and F: control group). Cell morphology was observed under an inverted microscope. The gap between cells increased, and the cells became reticulate after adding 75 pg/mL TGF-beta(2); also, the cells swelled and appeared spindle-shaped. However, antioxidants reduced these changes. Growth inhibition was analyzed at 12, 24, and 48 h, and the differences between groups were not statistically significant. Cell apoptosis was analyzed, and the differences between group A and groups B and C were statistically significant (P < 0.05). Reverse transcriptase-polymerase chain reaction was used to detect mRNA expression of alpha-SMA. The alpha-SMA mRNA level was greater in group A than in groups B and C (P < 0.05). TGF-beta(2) inhibited LEC proliferation and induced apoptosis and EMT. GSH and CAT inhibited apoptosis and EMT in LECs, and they had little effect on cell proliferation. Reactive oxygen species may be involved in cell apoptosis and EMT induced by TGF-beta(2) as a cell-signaling molecule.

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