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Abnormal control of lung branching in experimental esophageal atresia

Title
Abnormal control of lung branching in experimental esophageal atresia
Type
Article in International Scientific Journal
Year
2013
Authors
Fragoso AC
(Author)
FMUP
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Aras-Lopez R
(Author)
Other
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Martinez L
(Author)
Other
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Estevão-Costa J
(Author)
FMUP
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Tovar JA
(Author)
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Journal
Vol. 29 No. 2
Pages: 171-177
ISSN: 0179-0358
Publisher: Springer Nature
Indexing
Publicação em ISI Web of Science ISI Web of Science
Pubmed / Medline
Scientific classification
FOS: Medical and Health sciences
Other information
Authenticus ID: P-002-0XP
Abstract (EN): Esophageal atresia and tracheo-esophageal fistula (EA-TEF) result from abnormal division of the foregut into esophagus and trachea thus, it may influence airway branching and lung development. The present study examined lung morphogenesis in fetuses with EA-TEF focusing in the expression of FGF10 and its receptor FGFR2 IIIb. Pregnant rats received either 1.75 mg/kg i.p. adriamycin or vehicle on E7, E8 and E9. Embryos were recovered at E15, E18 and E21 and lungs processed for immunohistochemistry and RT-PCR. Three groups were studied: control, adriamycin-exposed with EA-TEF, and adriamycin-exposed without EA-TEF. Comparisons were performed with Mann-Whitney or t tests (significance level, 5 %). Lung weight at E15 and E18 were significantly lower in adriaEA fetuses in which the relative mRNA levels of FGF10 were significantly higher. These differences disappeared near term. The receptor FGFR2 IIIb messenger was only significantly increased in adria noEA fetuses at E15. Immunohistochemical study was consistent with these findings. Abnormal expression of FGF10 during earlier stages of development, when the lungs are smaller than controls, suggests a compensatory response aimed at "catching up" delayed tracheobronchial branching. Whether similar changes take place in the human condition and influence respiratory physiology remain to be determined.
Language: English
Type (Professor's evaluation): Scientific
No. of pages: 7
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