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Related Experiment Videos

Candidate genes controlling pulmonary function in mice: transcript profiling and predicted protein structure.

Koustav Ganguly1, Tobias Stoeger, Scott C Wesselkamper

  • 1National Research Center for Environment and Health (GSF), Institute for Inhalation Biology, Neuherberg, Germany.

Physiological Genomics
|September 7, 2007
PubMed
Summary
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This study identifies novel genes influencing lung function in mice, revealing superoxide dismutase 3 (SOD3) as a key factor in airway volume regulation, crucial for understanding asthma and COPD development.

Area of Science:

  • Genetics and Genomics
  • Pulmonary Medicine
  • Molecular Biology

Background:

  • Impaired lung development and reduced lung capacity are significant risk factors for asthma and chronic obstructive pulmonary disease (COPD).
  • Previous genomewide linkage analysis identified quantitative trait loci (QTLs) associated with lung function parameters like dead space volume (Vd), total lung capacity (TLC), lung compliance (CL), and diffusing capacity for CO (D(CO)) in mouse strains.

Purpose of the Study:

  • To identify and validate candidate genes within QTLs that influence lung function traits.
  • To investigate the role of specific genes, including superoxide dismutase 3 (SOD3), trefoil factor 2 (TFF2), and ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2), in determining lung capacity and airway volume.

Main Methods:

  • Comparative microarray analysis of lung transcript levels between C3H and JF1 mouse strains.

Related Experiment Videos

  • Exon sequencing of candidate genes across multiple mouse strains (C3H, BALB/cByJ, C57BL/6J, A/J, PWD/PhJ, JF1) to predict protein structure alterations.
  • Generation and phenotypic analysis of gene-targeted Sod3 knockout mice (Sod3(-/-)) to assess its role in lung function.

    • Main Results:

    • Microarray analysis revealed over 900 differentially expressed transcripts related to lung development, function, and remodeling between C3H and JF1 strains.
    • Three genes, SOD3, TFF2, and ENPP2, localized to relevant QTLs and showed differential expression or sequence polymorphisms potentially affecting protein structure.
    • Gene-targeted Sod3(-/-) mice exhibited increased conducting airway volume (Vd/TLC) compared to controls, supporting the role of SOD3 in airway regulation.

    Conclusions:

    • Two novel genes (TFF2 and ENPP2) and two suspected genes (SOD3 and Relaxin 1) have been identified as potential determinants of lung function in mice.
    • The study provides strong evidence that SOD3 is a significant contributing factor to the complex trait of conducting airway volume.
    • These findings advance the understanding of genetic underpinnings of lung function and may offer new targets for therapies related to respiratory diseases like asthma and COPD.