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The apelinergic system in the developing lung: expression and signaling.

Paulina Piairo1, Rute S Moura, Cristina Nogueira-Silva

  • 1Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.

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|October 22, 2011
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Summary

The apelinergic system regulates cardiovascular homeostasis and is involved in embryonic development. This study reveals apelin inhibits fetal lung growth by suppressing p38 and JNK signaling pathways.

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Area of Science:

  • Developmental Biology
  • Cardiovascular Physiology
  • Pulmonary Medicine

Background:

  • The apelin/APJ system is crucial for cardiovascular homeostasis and embryonic development, including vascular, ocular, and heart formation.
  • This system is highly expressed in pulmonary tissue, suggesting a potential role in lung development.

Purpose of the Study:

  • To investigate the role and function of the apelinergic system in fetal lung development.
  • To characterize the expression and localization of apelin and APJ in developing rat lungs.

Main Methods:

  • Immunohistochemistry and Western blot analysis were used to determine apelin and APJ expression and localization in fetal and adult rat lungs.
  • Fetal rat lung explants were cultured in vitro and treated with varying doses of apelin.
  • Morphometric analysis and MAPK signaling pathway assessment (p38, JNK phosphorylation) were performed on treated explants.

Main Results:

  • Both apelin and APJ are constitutively expressed in developing rat lungs, with APJ showing monomeric, dimeric, and oligomeric forms and nuclear localization in the pulmonary epithelium.
  • Apelin expression is higher in fetal lungs compared to adult lungs.
  • Apelin supplementation inhibited branching morphogenesis in a dose-dependent manner, correlating with decreased p38 and JNK phosphorylation.

Conclusions:

  • This study provides the first evidence of an active apelinergic system in fetal lung development.
  • Apelin appears to inhibit fetal lung growth by suppressing the p38 and JNK signaling pathways.