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Related Experiment Video

Updated: Jun 19, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
06:14

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LncRNA BANCR/miR-15a/MAPK1 Induces Apoptosis and Increases Proliferation of Vascular Smooth Muscle Cells in Aortic

Zihe Zheng1,2, Wei Wang1,2, Bo Chen1,2,3

  • 1Department of Cardiovascular Surgery, Fujian Medical University Union Hospital, Fuzhou, China.

Cell Biochemistry and Biophysics
|March 29, 2025
PubMed
Summary
This summary is machine-generated.

Long non-coding RNA BANCR promotes aortic dissection by activating the p38 MAPK pathway, increasing MMP2 expression, and affecting cell behavior. Targeting BANCR may offer new therapeutic strategies for aortic dissection.

Keywords:
LncRNA BANCRMMP2aortic dissectionceRNAvascular smooth muscle cells

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Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Area of Science:

  • Vascular Biology
  • Molecular Medicine
  • Genetics

Background:

  • Aortic dissection carries a high mortality rate, emphasizing the need for effective preventive strategies.
  • Long non-coding RNA (LncRNA) BANCR is a known regulator in other diseases, but its role in aortic dissection is unknown.
  • Understanding molecular mechanisms is crucial for developing targeted interventions.

Purpose of the Study:

  • To investigate the function and molecular mechanisms of LncRNA BANCR in aortic dissection.
  • To explore the involvement of the p38 MAPK pathway in BANCR-mediated effects.
  • To elucidate the ceRNA network involving BANCR in vascular smooth muscle cells.

Main Methods:

  • Isolation and characterization of vascular smooth muscle cells from aortic dissection samples.
  • Modulation of BANCR expression using transfection and small interfering RNA.
  • Assessment of p38 MAPK pathway activation using specific inhibitors.
  • Validation of competing endogenous RNA (ceRNA) network via dual luciferase assay.
  • Evaluation of cellular phenotypes including proliferation, migration, and apoptosis.

Main Results:

  • BANCR was overexpressed in aortic dissection tissues and cells.
  • BANCR activated the p38 MAPK pathway, leading to increased cell proliferation, migration, and apoptosis.
  • The LncRNA BANCR/miR-15a-5p/MAPK1 axis formed a ceRNA network regulating MMP2 expression via p38 MAPK.
  • BANCR overexpression upregulated MMP2, which was reversed by BANCR suppression or p38 MAPK inhibition.

Conclusions:

  • The LncRNA BANCR/miR-15a-5p/MAPK1 axis plays a critical role in aortic dissection pathogenesis.
  • BANCR promotes adverse cellular phenotypes in vascular smooth muscle cells through the p38 MAPK/MMP2 signaling pathway.
  • Targeting BANCR presents a potential therapeutic avenue for aortic dissection.