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Temporal RAGE Over-Expression Disrupts Lung Development by Modulating Apoptotic Signaling.

Derek M Clarke1, Madison N Kirkham1, Logan B Beck1

  • 1Department of Cell Biology and Physiology, Brigham Young University, 3054 Life Sciences Building, Provo, UT 84602, USA.

Current Issues in Molecular Biology
|December 27, 2024
PubMed
Summary

Receptors for advanced glycation end products (RAGE) significantly impact lung development. Early RAGE overexpression causes severe tissue loss and structural damage, highlighting its critical role in lung formation.

Keywords:
RAGEapoptosisembryolungtransgenic

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Receptors for advanced glycation end products (RAGE) are cell surface receptors abundant in lung tissue.
  • RAGE plays a role in various physiological and pathological processes.
  • Its specific role in lung development requires further elucidation.

Purpose of the Study:

  • To investigate the role of RAGE in lung development using a transgenic mouse model.
  • To determine the impact of spatiotemporal RAGE overexpression on lung histology and molecular pathways.

Main Methods:

  • Utilized a transgenic (TG) mouse model with controlled RAGE overexpression.
  • Performed histological imaging to assess lung structure.
  • Analyzed molecular markers of apoptosis, cell survival, and cell cycle regulation.

Main Results:

  • RAGE upregulation from embryonic day (E) 15.5 to E18.5 led to thickened alveolar parenchyma and reduced surface area.
  • RAGE overexpression from E0 to E18.5 resulted in significant tissue loss and architectural disruption.
  • Mitochondrial dysfunction, dysregulated intrinsic and extrinsic apoptosis, and altered cell survival/cycle pathways were observed.

Conclusions:

  • RAGE is a pivotal modulator of lung development.
  • The timing of RAGE upregulation critically influences lung development outcomes and histological phenotypes.
  • RAGE signaling may contribute to developmental lung diseases.