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Midkine expression is associated with postnatal development of the lungs
Onrai Matsuura1, Kenji Kadomatsu, Yoshifumi Takei
1Department of Biochemistry, Nagoya University School of Medicine, Japan.
Cell Structure and Function
|September 11, 2002
Summary
Midkine protein expression increases during early lung development in mice. However, hyperoxia exposure impairs lung development and suppresses midkine in neonates, but not in adults.
Area of Science:
- Cell Biology
- Developmental Biology
- Pulmonary Medicine
Background:
- Midkine is a heparin-binding growth factor produced by a retinoic acid-responsive gene.
- Retinol is crucial for lung development and treating bronchopulmonary dysplasia.
- Midkine influences lung explant maturation and offers cytoprotection.
Purpose of the Study:
- To investigate midkine expression during postnatal lung development.
- To examine midkine's role in hyperoxic lung injury in neonatal and adult mice.
Main Methods:
- Quantified midkine protein levels during postnatal development.
- Utilized immunohistochemistry to localize midkine in lung tissues.
- Exposed neonatal and adult mice to hyperoxia (>95% oxygen).
- Assessed retinoic acid's effect on midkine expression.
Main Results:
- Midkine protein peaked around postnatal day 4 in alveolar cells.
- Hyperoxia impaired neonatal lung development and suppressed midkine expression.
- Adult lungs and lung adenocarcinoma cells showed no change in midkine expression under hyperoxia.
- Retinoic acid significantly induced midkine in neonatal lungs.
Conclusions:
- Midkine expression is linked to normal postnatal lung development.
- Midkine is not essential for hyperoxic cell damage response in adult lungs.
- Neonatal midkine expression is sensitive to hyperoxia and responsive to retinoic acid.