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Regulation of Eaf2 in mouse lens cells apoptosis induced by ultraviolet radiation
Fan Xiao1, Jin-Song Zhang, Jiang-Yue Zhao
1Department of Ophthalmology, the Fourth Affiliated Hospital of China Medical University, Shenyang 110005, Liaoning Province, China.
Aim:
To investigate the regulation of Eaf2 protein in mouse lens cells apoptosis induced by ultraviolet (UV) radiation.
Methods:
An eye of Eaf2 gene knockout mice or normal control mice was exposed to UV radiation, and the other one was non-exposed. All of lenses were analyzed by TUNEL and caspase 3 activity assays to determine the difference of the apoptosis induced by UV radiation. In addition, exposed and non-exposed lenses were analyzed by quantified p53 expression and real-time reverse transcription-polymerase chain reaction (RT-PCR) of Bax, Bid, Apaf-1, Puma and Noxa, to compare Eaf2 gene knockout mice and normal control mice.
Results:
UV radiation caused apoptosis of lens cells in normal control mice and Eaf2 knockout mice. Activity of caspase 3 was significantly higher in normal control mice than Eaf2 knockout mice. Expression of p53 protein was significantly higher in lenses exposed to UV radiation than nonexposed lenses, but was similar between Eaf2 gene knockout mice and normal control mice in the same UV condition. After exposing to UV radiation, the analysis of real-time RT-PCR demonstrated that mRNA levels of Puma and Noxa were significantly higher in lenses of normal control mice than Eaf2 gene knockout mice, and that mRNA levels of Bax, Bid and Apaf-1 were not significantly different between gene knockout mice and normal control mice.
Conclusion:
Eaf2 increases lens cells apoptosis induced by ultraviolet radiation. And Eaf2 up-regulates expression of the Puma and the Noxa to act on lens cells apoptosis after UV radiation.
Insights
Eaf2 protein enhances ultraviolet radiation-induced apoptosis in mouse lens cells by up-regulating Puma and Noxa. This finding is crucial for understanding UV-induced eye damage and developing protective strategies.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Ultraviolet (UV) radiation poses a significant threat to ocular health, potentially inducing apoptosis in lens cells.
- The precise molecular mechanisms regulating UV-induced lens cell apoptosis are not fully understood.
- Eaf2 protein's role in this process requires further investigation.
Purpose of the Study:
- To investigate the regulatory role of Eaf2 protein in mouse lens cell apoptosis following UV radiation exposure.
- To compare the effects of UV radiation on lens cells in Eaf2 gene knockout mice versus normal control mice.
Main Methods:
- UV radiation exposure was applied to the eyes of Eaf2 gene knockout and normal control mice.
- Apoptosis was assessed using TUNEL assays and caspase 3 activity.
- Gene and protein expression levels (p53, Bax, Bid, Apaf-1, Puma, Noxa) were analyzed via real-time RT-PCR and protein quantification.
Main Results:
- UV radiation induced apoptosis in lens cells of both normal and Eaf2 knockout mice.
- Caspase 3 activity was significantly higher in normal mice compared to Eaf2 knockout mice.
- While p53 expression increased with UV exposure, it was similar between groups. mRNA levels of Puma and Noxa were significantly higher in normal mice post-UV exposure, unlike Bax, Bid, and Apaf-1.
Conclusions:
- Eaf2 protein plays a role in promoting UV-induced apoptosis in lens cells.
- Eaf2 up-regulates the expression of Puma and Noxa, contributing to UV-induced lens cell apoptosis.
