Long Non-Coding RNA-ATB Attenuates the Angiotensin II-Induced Injury of Vascular Endothelial Cell

Miao Wang1, Shouyi Gan1, Bin Li1

  • 1Deparment of Cardiovascular Medicine, Xian Ning Central Hospital, the First Affiliated Hospital of Hubei University of Science and Technology, Xian Ning Central Hospital, Xian'an District, Xian Ning City, Hubei Province, China.

Abstract

Insights

Long noncoding RNA activated by transforming growth factor-II (lncRNA-ATB) plays a protective role in endothelial cell injury. Lower lncRNA-ATB levels correlate with cardiovascular disease development, impacting cell viability and apoptosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Long noncoding RNA activated by transforming growth factor-II (lncRNA-ATB) is implicated in various cancers.
  • The role of lncRNA-ATB in cardiovascular disease and endothelial cell injury remains largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of lncRNA-ATB in endothelial cell injury.
  • To elucidate the potential involvement of lncRNA-ATB in cardiovascular disease pathogenesis.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were subjected to Angiotensin II (Ang II)-induced injury.
  • lncRNA-ATB expression was quantified using qRT-PCR.
  • Cell viability and apoptosis were assessed via CCK-8 assay and flow cytometry.

Main Results:

  • Ang II treatment significantly downregulated lncRNA-ATB expression in HUVECs.
  • Knockdown of lncRNA-ATB exacerbated Ang II-induced endothelial cell injury, impairing viability and increasing apoptosis.
  • Overexpression of lncRNA-ATB demonstrated protective effects, inhibiting apoptosis and restoring cell viability.

Conclusions:

  • lncRNA-ATB expression is reduced during endothelial cell injury induced by Ang II.
  • lncRNA-ATB exhibits protective functions against endothelial cell injury.
  • These findings suggest lncRNA-ATB is a potential therapeutic target for cardiovascular disease.

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