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An Experimental System to Study Mechanotransduction in Fetal Lung Cells
09:35

An Experimental System to Study Mechanotransduction in Fetal Lung Cells

Published on: February 16, 2012

Adult onset lung disease following transient disruption of fetal stretch-induced differentiation

Joseph J Hudak1, Erin Killeen, Ashok Chandran

  • 1The Brady Laboratory, Section of Neonatology, Department of Pediatrics, Stony Brook University, School of Medicine, Stony Brook, New York, 11794, USA. joseph.hudak@us.army.mil

Respiratory Research
|May 8, 2009
PubMed

Insights

Disrupting fetal lung development with gene therapy in rats caused progressive respiratory problems in adulthood. This highlights how early developmental changes can lead to adult-onset lung disease.

Area of Science:

  • Developmental Biology
  • Pulmonary Medicine
  • Genetics

Background:

  • Adult diseases can originate from fetal development disruptions.
  • In utero organogenesis interference can lead to long-term health issues.

Purpose of the Study:

  • To investigate respiratory function changes in aging rats after transient in utero lung growth disruption.
  • To examine the long-term effects of fetal gene interference on lung development and function.

Main Methods:

  • Fetal rats were treated in utero with an adenovirus carrying an anti-sense CFTR gene fragment.
  • Respiratory function was assessed in aging rats using lung function tests and pressure-volume curves.
  • Lung structural changes were analyzed using morphometric analysis.

Main Results:

  • In utero-treated rats showed abnormal lung function from 30 days of age, worsening with age.
  • Pulmonary function abnormalities included decreased static compliance and increased airway resistance, damping, and elastance.
  • Pressure-volume curves indicated impaired lung inflation and air trapping; these correlated with structural lung changes.

Conclusions:

  • Transient disruption of lung organogenesis via single gene interference can cause progressive changes in lung function and structure.
  • Subtle alterations in gene expression during fetal development can result in adult-onset lung disease.
  • This study provides a model for understanding fetal origins of adult respiratory diseases.

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