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Related Experiment Video

Updated: May 23, 2026

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
07:37

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Published on: July 14, 2016

miR‑16‑5p Protects RGCs Against Retinal Ischemia-Reperfusion Injury by Modulating Astrocyte-Mediated

Wen Hu1, Wenjing He1, Guangyi Huang1,2

  • 1Department of Ophthalmology, The People's Hospital of Guangxi Zhuang Autonomous Region & Guangxi Key Laboratory of Eye Health & Guangxi Health Commission Key Laboratory of Ophthalmology and Related Systemic Diseases Artificial Intelligence Screening Technology & Institute of Ophthalmic Diseases, Guangxi Academy of Medical Sciences, Guangxi Zhuang Autonomous Region, Nanning, 530021, China.

Molecular Neurobiology
|May 21, 2026
PubMed

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Summary

MicroRNA-16-5p protects retinal ganglion cells from injury by reducing astrocyte inflammation through the Wip1/NF-κB pathway. This study clarifies miR-16-5p

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Molecular Biology

Background:

  • Astrocyte-mediated neuroinflammation is a key factor in retinal neurodegeneration after ischemia-reperfusion (IR) injury.
  • The specific role of microRNA-16-5p (miR-16-5p) in this inflammatory process is not well understood.
  • Understanding miR-16-5p's function is crucial for developing targeted therapies for retinal IR injury.

Purpose of the Study:

  • To investigate the function and underlying mechanism of miR-16-5p in retinal IR injury.
  • To determine if miR-16-5p modulates astrocyte activation and neuroinflammation.
  • To elucidate the signaling pathway involved in miR-16-5p's protective effects.

Main Methods:

  • Predicted and validated miR-16-5p targets using TargetScan and RNA pull-down assays.
Keywords:
AstrocytesMiR-16-5pNF-κBRetina NeuroinflammationRetinal ischemia–reperfusionWip1

Related Experiment Videos

Last Updated: May 23, 2026

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
07:37

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Published on: July 14, 2016

  • Assessed miR-16-5p expression in IR-injured retinas and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated astrocytes.
  • Modulated miR-16-5p levels in vitro and in vivo to examine effects on astrocyte activation, inflammatory cytokines, Wip1/NF-κB signaling, RGC apoptosis, retinal function, and morphology.

    • Main Results:

    • miR-16-5p was predicted to target and decrease wild-type p53-induced phosphatase 1 (Wip1) expression.
    • miR-16-5p expression was significantly downregulated in IR retinas and OGD/R astrocytes, correlating with increased astrocyte activation, pro-inflammatory cytokines (TNF-α, IL-1β), Wip1, and phosphorylated NF-κB p65 (p-p65).
    • miR-16-5p mimics ameliorated IR-induced retinal injury, including RGC apoptosis and functional/morphological deficits, while inhibitors worsened these outcomes.

    Conclusions:

    • miR-16-5p plays a protective role against retinal IR injury.
    • It suppresses astrocyte-mediated inflammation by targeting Wip1 and inhibiting the Wip1/NF-κB signaling axis.
    • miR-16-5p represents a potential therapeutic target for mitigating neuroinflammation and protecting retinal ganglion cells following IR injury.