Mechanism research of miR-181 regulating human lens epithelial cell apoptosis
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National Natural Science Foundation of China(No.81270988, 81470617); Scientific Research Project of Education Department, Liaoning Province(No. L2014305)

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    Abstract:

    AIM: To investigate the expression of miR-181 in the lens tissue of cataract and the regulating mechanism of miR-181 on apoptosis of human lens epithelial cell.

    METHODS:Real time q-PCR was used to measure the expression of miR-181 in the anterior lens capsules of age-related cataract and human lens epithelial cell apoptosis model. miR-181 mimic and inhibitor were transfected using Lipofectamine 2 000 to regulate the expression of miR-181, and then Real time q-PCR was used to verify transfection efficiency. Flow cytometry was used to detect the change of cell apoptosis rate.

    RESULTS: Compared with control group, the expression of miR-181 was significantly higher in both the anterior lens capsules of age-related cataract and human lens epithelial cell apoptosis model; the relative expression of miR-181 in lens epithelial cells transfected with miR-181 mimic was increased, whereas decreased in cells transfected with miR-181 inhibitor; the apoptosis rate of cells transfected with miR-181 mimic was increased, while reduced in miR-181 inhibitor group. Each result was statistically significant(P<0.01).

    CONCLUSION: High expression of miR-181 is detected in anterior lens capsule of age-related cataract. miR-181 might play a certain role in the pathogenesis of cataract via promoting human lens epithelial cell apoptosis. miR-181 probably becomes a new approach for the nonoperative treatment of cataract, but the concrete mechanism still needs to be further studied.

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Yu Qin, Jiang-Yue Zhao, Wen-Ting Luo, et al. Mechanism research of miR-181 regulating human lens epithelial cell apoptosis. Guoji Yanke Zazhi( Int Eye Sci) 2015;15(5):759-763

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Publication History
  • Received:February 25,2015
  • Revised:April 13,2015
  • Adopted:
  • Online: May 05,2015
  • Published: