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Related Experiment Video

Updated: Jul 1, 2026

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

Published on: October 10, 2012

Protection of Islet Beta Cells from Iron Overload-Induced Injury by Long Non-Coding RNA Maternally Expressed Gene 3.

Hong Liang¹, Jianming Luo²

¹Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University; Department of Pediatrics, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University).

Journal of Visualized Experiments : Jove

|June 29, 2026

Summary

Maternally expressed gene 3 (MEG3) downregulation worsens iron-induced islet cell damage in beta-thalassemia major. Reduced MEG3 enhances apoptosis via the NF-kappa B pathway, contributing to glucose metabolism issues.

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Last Updated: Jul 1, 2026

Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer

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Published on: May 14, 2019

Area of Science:

Endocrinology
Molecular Biology
Genetics

Background:

Beta-thalassemia major (β-TM) patients often experience abnormal glucose metabolism due to factors like iron overload and inflammation.
Long non-coding RNAs (lncRNAs) are critical regulators of cellular processes, including apoptosis and glucose homeostasis.
Pancreatic islet dysfunction is a key complication in β-TM, necessitating research into its underlying molecular mechanisms.

Purpose of the Study:

To investigate the role of the lncRNA maternally expressed gene 3 (MEG3) in iron-induced pancreatic islet β-cell injury.
To elucidate the molecular pathways through which MEG3 influences β-cell apoptosis under conditions of iron overload.

Main Methods:

An iron-overload mouse model was established using intraperitoneal iron dextran injections.
Pancreatic tissue iron deposition and damage were assessed using Prussian blue and H&E staining.
MEG3 expression was quantified by RT-PCR, and in vitro studies used MIN6 cells with MEG3 knockdown via small interfering RNA.
Apoptosis was measured by flow cytometry, and NF-kappa B signaling pathway activation was analyzed by Western blotting.

Main Results:

Iron overload induced significant pancreatic iron deposition and structural damage in mice.
MEG3 expression was markedly reduced in the pancreas of iron-overloaded mice.
In vitro, MEG3 knockdown in MIN6 cells led to increased apoptosis and activation of the NF-kappa B signaling pathway.

Conclusions:

Downregulation of MEG3 exacerbates iron-induced islet β-cell apoptosis, likely through activation of the NF-kappa B signaling pathway.
MEG3 appears to exert a protective effect against iron-induced β-cell apoptosis, potentially by modulating the NF-kappa B pathway.
This MEG3-mediated mechanism may contribute to the observed islet dysfunction and abnormal glucose metabolism in β-TM patients with iron overload.