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Angiogenesis-related gene expression profiling in ventilated preterm human lungs
Monique E De Paepe1, David Greco, Quanfu Mao
1Department of Pathology, Women and Infants Hospital, Providence, Rhode Island 02905, USA. mdepaepe@wihri.org
Experimental Lung Research
|August 20, 2010
Summary
Mechanical ventilation in preterm infants with bronchopulmonary dysplasia (BPD) alters lung angiogenesis gene expression. Ventilated lungs show increased antiangiogenic factors and decreased proangiogenic factors, impacting lung development.
Area of Science:
- Neonatal Medicine
- Pulmonary Biology
- Molecular Medicine
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disorder in preterm infants, linked to oxygen and mechanical ventilation.
- Pathological angiogenesis, specifically nonsprouting and dysmorphic microvascular growth, is a hallmark of BPD, but its molecular regulation is not fully understood.
Purpose of the Study:
- To investigate the gene expression profile of angiogenesis in the lungs of preterm infants exposed to short-term mechanical ventilation.
- To identify molecular regulators contributing to the arrested alveolar development and aberrant angiogenesis in BPD.
Main Methods:
- Focused microarray analysis of postmortem lung samples from ventilated preterm infants (24-27 weeks' gestation) and age-matched controls.
- Validation of key gene expression changes using real-time polymerase chain reaction (PCR) and immunolocalization.
Main Results:
- Differential expression of 13 out of 112 angiogenesis-related genes was observed.
- Up-regulated genes in ventilated lungs included antiangiogenic factors (thrombospondin-1, collagen XVIII alpha-1, TIMP1) and others like endoglin and CCL2.
- Down-regulated genes included proangiogenic factors (angiogenin, midkine) and key signaling molecules (VEGF-B, TEK/Tie-2).
Conclusions:
- Short-term ventilation induces a significant shift in lung angiogenic gene expression, favoring antiangiogenic and antisprouting regulators.
- This altered angiogenic profile may play a crucial role in the dysmorphic angiogenesis and impaired alveolarization characteristic of BPD.
