September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
MicroRNA-34a promotes apoptosis of human lens epithelial cells through down-regulation of Bcl-2 and SIRT1
Author Affiliations & Notes
  • Hongyang Zhang
    Guangdong General Hospital, San Gabriel, California, United States
  • QINGLAN LI
    Guangdong General Hospital, San Gabriel, California, United States
  • Yongjie Qin
    Guangdong General Hospital, San Gabriel, California, United States
  • Haike Guo
    Aier Eye Hospital, Zhengzhou, China
  • Footnotes
    Commercial Relationships   Hongyang Zhang, None; QINGLAN LI, None; Yongjie Qin, None; Haike Guo, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 2031. doi:
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      Hongyang Zhang, QINGLAN LI, Yongjie Qin, Haike Guo; MicroRNA-34a promotes apoptosis of human lens epithelial cells through down-regulation of Bcl-2 and SIRT1. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2031.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : To investigate the role of microRNA-34a(miR-34a) in the induction of apoptosis of human lens epithelial cells.

Methods : The apoptosis in human lens epithelial (HLE-B3) cells was detected by Annexin V-PE apoptosis detection kit after the treatment with 200 μM H2O2 for 24 hours and lentiviral miR-34a vector transfection. The expression of miR-34a in HLE-B3 cells was quantified by qRT-PCR in response to H2O2 exposure and lentiviral miR-34a vector transfection. The effects of overexpression of miR-34a on the expression of B-cell lymphoma-2 (Bcl-2) and silent information regulator 1 (SIRT1) was determined by qRT-PCR and Western blot.

Results : The expression of miR-34a was up-regulated by the treatment of H2O2 in HLE-B3 cells. The increased expression of miR-34a is accompanied with the cell apoptosis. Consistence with the H2O2 exposure, ectopic overexpression of miR-34a in HLE-B3 cells promoted cells apoptosis. Importantly the anti-apoptosis factors Bcl-2 and SIRT1 were reduced significantly by up-regulation of miR-34a in HLE-B3 cells.

Conclusions : MiR-34a promotes apoptosis of human lens epithelial cells by down-regulating Bcl-2 and SIRT1, suggesting that miR-34a may involve in the pathogenesis of cataract formation and targeting miR-34a may be potentially therapeutic approach for the treatment of cataract.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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