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Cell Physiol Biochem. 2018;50(1):246-260. doi: 10.1159/000494003. Epub 2018 Oct 4.

Long Non-Coding RNA H19 Regulates Human Lens Epithelial Cells Function.

Liu X1,2,3, Liu C4,3,5, Shan K4,3, Zhang S4,2,3, Lu Y1,2,3, Yan B4,2,3, Luo Y1,2,3.

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Department of Ophthalmology, Eye and ENT Hospital of Fudan University, Shanghai, China.
Key NHC Key Laboratory of Myopia (Fudan University), Laboratory of Myopia, Chinese Academy of Medical Sciences, Shanghai, China.
Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, Shanghai, China.
Research Center, Eye and ENT Hospital of Fudan University, Shanghai, China.
The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.



Age-related cataract (ARC) remains the leading cause of visual impairment among the elderly population. Long non-coding RNAs (lncRNAs) have emerged as potential regulators in many ocular diseases. However, the role of lncRNAs in nuclear ARC, a subtype of ARC, requires further elucidation.


LncRNA sequencing was performed to identify differentially expressed lncRNAs between the capsules of transparent and nuclear ARC lenses. Expression validation was confirmed by qRT-PCR. MTT assay, Calcein-AM and propidium iodide double staining, Rhodamine 123 and Hoechst double staining, EdU and transwell assay were used to determine the role of H19 or miR-675 in the viability, apoptosis, proliferation and migration of primary cultured human lens epithelial cells (HLECs). Bioinformatics and luciferase reporter assays were used to identify the binding target of miR-675.


Sixty-three lncRNAs are differentially expressed between the capsules of transparent and nuclear ARC lenses. One top abundantly expressed lncRNA, H19, is significantly up-regulated in the nuclear ARC lens capsules and positively associated with nuclear ARC grade. H19 knockdown accelerates apoptosis development and reduces the proliferation and migration of HLECs upon oxidative stress. H19 is the precursor of miR-675, and a reduction of H19 inhibits miR-675 expression. miR-675 regulates CRYAA expression by targeting the binding site within the 3'UTR. Moreover, miR-675 increases the proliferation and migration while decreasing the apoptosis of HLECs upon oxidative stress.


H19 regulates HLECs function through miR-675-mediated CRYAA expression. This finding would provide a novel insight into the pathogenesis of nuclear ARC.


CRYAA; Long non-coding RNA; Nuclear age-related cataract; miRNA

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