Hsa_circ_0081065 exacerbates IH-induced EndMT via regulating miR-665/HIF-1α signal axis and HIF-1α nuclear

Shan Jiang1, Xiaowei Xing2, Ming Hong2

  • 1Department of Emergency, The Second Hospital of Shandong University, Shandong, China.

Scientific Reports
|January 10, 2024
PubMed

Insights

Intermittent hypoxia (IH) upregulates hsa_circ_0081065 in endothelial cells, promoting EndMT by sponging miR-665 to increase HIF-1α. This highlights hsa_circ_0081065 as a therapeutic target for IH-related conditions.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genomics

Background:

  • Circular RNAs (circRNAs) are crucial in biological processes, but their role in intermittent hypoxia (IH) is unclear.
  • Intermittent hypoxia (IH) is linked to various pathologies, and understanding its molecular mechanisms is vital.

Purpose of the Study:

  • To elucidate the molecular mechanism of circRNAs in intermittent hypoxia (IH).
  • To investigate the function of hsa_circ_0081065 in IH-induced endothelial to mesenchymal transition (EndMT).

Main Methods:

  • Transcriptome sequencing identified differentially expressed circRNAs in an IH model.
  • RT-qPCR, FISH, RNA-pull down, RIP, EMSA, and dual-luciferase reporter assays were employed.
  • EndMT markers and HIF-1α nuclear translocation were assessed.

Main Results:

  • 73 circRNAs were differentially expressed under IH, with hsa_circ_0081065 significantly upregulated.
  • Hsa_circ_0081065, localized in the cytoplasm, promoted EndMT.
  • Hsa_circ_0081065 sponges miR-665, upregulating HIF-1α and its nuclear translocation.

Conclusions:

  • Hsa_circ_0081065 exacerbates IH-induced EndMT via the miR-665/HIF-1α axis.
  • Targeting hsa_circ_0081065 offers a potential therapeutic strategy for IH-related diseases like Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS).

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