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

Xin Liu1,2,3, Chang Liu4,3,5, Kun Shan4,3

  • 1Department of Ophthalmology, Eye and ENT Hospital of Fudan University, Shanghai, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|October 5, 2018
PubMed
Summary
This summary is machine-generated.

Long non-coding RNA H19 regulates human lens epithelial cell function via miR-675, impacting nuclear age-related cataract (ARC) development. This study reveals a novel mechanism in ARC pathogenesis.

Keywords:
CRYAALong non-coding RNANuclear age-related cataractmiRNA

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Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Age-related cataract (ARC) is a primary cause of visual impairment in older adults.
  • Long non-coding RNAs (lncRNAs) are implicated in ocular diseases, but their role in nuclear ARC is not well understood.

Purpose of the Study:

  • To investigate the role of lncRNAs, specifically H19, in the pathogenesis of nuclear ARC.
  • To elucidate the regulatory pathway involving H19, miR-675, and CRYAA in human lens epithelial cells (HLECs).

Main Methods:

  • LncRNA sequencing to identify differentially expressed lncRNAs in nuclear ARC lens capsules.
  • Quantitative real-time PCR (qRT-PCR) for expression validation.
  • Cellular assays (MTT, Calcein-AM/PI, Rhodamine 123/Hoechst, EdU, Transwell) to assess HLEC viability, apoptosis, proliferation, and migration.
  • Bioinformatics and luciferase reporter assays to determine miR-675 targets.

Main Results:

  • H19 was significantly upregulated in nuclear ARC lens capsules and associated with ARC grade.
  • H19 knockdown increased HLEC apoptosis and decreased proliferation/migration under oxidative stress.
  • H19 is a precursor to miR-675, which targets CRYAA and promotes HLEC proliferation/migration while reducing apoptosis.

Conclusions:

  • H19 regulates HLEC function through the miR-675-mediated CRYAA pathway.
  • This pathway offers new insights into the molecular mechanisms underlying nuclear ARC development.