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Author Spotlight: Establishment and Confirmation of a Postnatal Right Ventricular Volume Overload Mouse Model
06:04

Author Spotlight: Establishment and Confirmation of a Postnatal Right Ventricular Volume Overload Mouse Model

Published on: June 9, 2023

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Downregulated developmental processes in the postnatal right ventricle under the influence of a volume overload

Chunxia Zhou1, Sijuan Sun2, Mengyu Hu3

  • 1Department of Thoracic and Cardiovascular Surgery, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Cell Death Discovery
|August 8, 2021
PubMed

Insights

Volume overload reactivates the cell cycle in the developing mouse right ventricle (RV). This contrasts with normal development, suggesting a novel mechanism for RV adaptation to stress in congenital heart disease.

Area of Science:

  • Cardiovascular Research
  • Developmental Biology
  • Molecular Cardiology

Background:

  • Postnatal mouse ventricular development involves downregulated cardiac regeneration.
  • The right ventricle (RV) exhibits distinct characteristics compared to the left ventricle.
  • The impact of volume overload (VO) on RV development, particularly in pediatric congenital heart disease, remains poorly understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which prepubertal RV volume overload affects postnatal mouse RV development.
  • To identify key pathways and cellular processes altered by RV VO.

Main Methods:

  • A mouse model was established to induce RV VO by creating an aortocaval fistula on postnatal day 7.
  • RNA sequencing (RNAseq) was performed on RV tissues from postnatal day 14 to 21.
  • Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted.

Main Results:

  • Angiogenesis was the most enriched GO term in both sham and VO groups.
  • Regulation of the mitotic cell cycle emerged as a significantly enriched GO term in the VO group, but not in the sham group.
  • A ~20-fold increase in Ki67-positive cardiomyocytes was observed in the VO group, indicating enhanced cell proliferation. KEGG analysis revealed a shift from peroxisome proliferators-activated receptor (PPAR) signaling to cell cycle pathways due to VO.

Conclusions:

  • Volume overload reactivates the cell cycle in the developing mouse right ventricle.
  • Angiogenesis remains a key process, but cell cycle regulation is significantly altered under VO conditions.
  • The observed effects may be mediated by the replacement of the PPAR signaling pathway with the cell cycle pathway in response to RV VO.

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