Signaling molecules in the fetal rabbit model for congenital diaphragmatic hernia.

Abstract:

RATIONALE AND OBJECTIVES:Little is known about molecular changes in lungs of fetal rabbits with surgically induced diaphragmatic hernia (DH). Therefore, we examined in this model gene expressions of pivotal molecules for the developing lung. METHODS:At day 23 of gestation, DH was created in 12 fetuses from 4 does. Both lungs from six live DH fetuses and from six unoperated controls were harvested and weighed at term. Transcription of 15 genes involved in alveolarization, angiogenesis, regulation of vascular tone, or epithelial maturation was investigated by real-time quantitative polymerase chain reaction. MAIN RESULTS:DH decreased lung-to-body weight ratio (P < 0.001). A bilateral downregulation was seen for genes encoding for tropoelastin (P < 0.01), lysyl oxidase (P < 0.05), fibulin 5 (P < 0.05), and cGMP specific phosphodiesterase 5 (P < 0.05). Lower mRNA levels for endothelial nitric oxide synthase occurred in the ipsilateral lung (P < 0.05). CONCLUSIONS:Experimental DH in fetal rabbits disrupted transcription of genes implicated in lung growth and function. Similarities with the human disease make this model appropriate for investigation of new prenatal therapies.

journal_name

Pediatr Pulmonol

journal_title

Pediatric pulmonology

authors

Vuckovic A,Roubliova XI,Votino C,Naeije R,Jani JC

doi

10.1002/ppul.22512

subject

Has Abstract

pub_date

2012-11-01 00:00:00

pages

1088-96

issue

11

eissn

8755-6863

issn

1099-0496

journal_volume

47

pub_type

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