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Related Concept Videos

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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: Dec 30, 2025

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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Long non-coding RNA MEG3 mediates high glucose-induced endothelial cell dysfunction.

Zhiqiang Wang1,2, Lili Ding1,3, Jun Zhu2,4

  • 1Department of Public Health, Xinjiang Medical University Urumqi, Xinjiang, China.

International Journal of Clinical and Experimental Pathology
|January 16, 2020
PubMed
Summary

Long noncoding RNA MEG3 is downregulated in diabetes-induced endothelial dysfunction. Its knockdown worsens inflammation and alters cell survival pathways, suggesting MEG3 as a therapeutic target.

Keywords:
MEG3diabetes mellitusendothelial dysfunctionlong noncoding RNA

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Area of Science:

  • Molecular Biology
  • Genetics
  • Endocrinology

Background:

  • Long noncoding RNAs (lncRNAs) are involved in diabetes mellitus (DM) progression and associated endothelial dysfunction.
  • Maternally expressed gene 3 (MEG3) is an lncRNA with proposed tumor suppressor functions.

Purpose of the Study:

  • To investigate the role of MEG3 as a regulator and biomarker in high glucose-induced endothelial dysfunction.
  • To explore MEG3's impact on endothelial cell behavior and signaling pathways under hyperglycemic conditions.

Main Methods:

  • Utilized small interfering RNA (siRNA) to knockdown lncRNA MEG3 in endothelial cells.
  • Assessed gene and protein expression via quantitative RT-PCR (qPCR) and Western blot.
  • Measured apoptosis and cell viability using flow cytometry and MTT assay, respectively.

Main Results:

  • MEG3 was significantly downregulated in a cellular model of hyperglycemia.
  • MEG3 knockdown exacerbated inflammatory damage and altered apoptosis/proliferation markers (Bcl-2, Bax, caspase-3, P53).
  • MEG3 knockdown activated TGF-β and Wnt/β-catenin signaling pathways.

Conclusions:

  • lncRNA MEG3 plays a crucial role in high glucose-induced endothelial dysfunction.
  • MEG3 functions as a potential therapeutic target and molecular biomarker for diabetic endothelial complications.