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LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3

Yong Jiang1, Chun-Hui Xu2, Ying Zhao3

  • 1Department of Laboratory Medicine, Jilin Medical University, Jilin . jiangyongpost@sina.com.

European Journal of Histochemistry : EJH
|January 17, 2023
PubMed

Insights

Long noncoding RNA LINC00926 worsens endothelial cell dysfunction in coronary heart disease by regulating the miR-3194-5p/JAK1/STAT3 pathway under hypoxia.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Vascular endothelial cell (VEC) dysfunction contributes to coronary heart disease (CHD).
  • Long noncoding RNA (lncRNA) LINC00926 is dysregulated in CHD patients, but its role remains unclear.
  • Understanding LINC00926's function in endothelial cells under stress is crucial.

Purpose of the Study:

  • To investigate the regulatory mechanism of LINC00926 in human umbilical vein endothelial cells (HUVECs) exposed to hypoxia.
  • To elucidate the role of LINC00926 in endothelial cell dysfunction.

Main Methods:

  • Hypoxia exposure of HUVECs (5% O2 for 24 h).
  • RT-qPCR and Western blotting for gene and protein expression.
  • CCK-8, flow cytometry, Transwell, and angiogenesis assays for cell function.
  • Bioinformatics and dual-luciferase reporter assays to confirm molecular interactions.

Main Results:

  • LINC00926 expression was elevated in CHD patients and hypoxia-exposed HUVECs.
  • Overexpression of LINC00926 impaired HUVEC proliferation, migration, and tube formation, while increasing apoptosis.
  • LINC00926 targets miR-3194-5p, which in turn targets JAK1, modulating the JAK1/STAT3 pathway.

Conclusions:

  • LINC00926 exacerbates endothelial cell dysfunction in hypoxia via the miR-3194-5p/JAK1/STAT3 signaling axis.
  • This finding highlights LINC00926 as a potential therapeutic target for CHD-related endothelial dysfunction.

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