Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/67937

TitleIL-6 is constitutively expressed during lung morphogenesis and enhances fetal lung explant branching
Author(s)Silva, Cristina Isabel Nogueira
Santos, Marta
Baptista, Maria J.
Moura, Rute S.
Correia-Pinto, Jorge
KeywordsAnimals
Female
Fetus
Gene Expression Regulation, Developmental
In Situ Hybridization
Interleukin-6
MAP Kinase Signaling System
Mitogen-Activated Protein Kinases
Random Allocation
Rats
Rats, Sprague-Dawley
Lung
Morphogenesis
Issue dateNov-2006
PublisherSpringer Nature
JournalPediatric Research
CitationNogueira-Silva, C., Santos, M., Baptista, M. J., Moura, R. S., & Correia-Pinto, J. (2006). IL-6 is constitutively expressed during lung morphogenesis and enhances fetal lung explant branching. Pediatric research, 60(5), 530-536
Abstract(s)Previous studies have shown that chorioamnionitis, with increased IL-6, promotes fetal lung maturation and decreases the incidence of respiratory distress syndrome in premature neonates. However, the expression pattern and the effects of IL-6 on fetal lung growth mechanisms remain unknown. IL-6 expression was assessed by in situ hybridization and by real-time PCR between 14.5 and 21.5 d postconception. Normal and nitrofen-induced hypoplastic lung explants were cultured with increasing IL-6 doses or IL-6 neutralizing antibodies. Branching, cellular proliferation (Ki-67) and MAPK phosphorylation in fetal lung explants were analyzed. Pulmonary primitive epithelium expressed IL-6 constitutively throughout all gestational ages, displaying highest levels during earliest stages. In normal and hypoplastic lung explants, IL-6 neutralizing antibodies significantly reduced, whereas IL-6 supplementation induced a biphasic effect (lower doses increased, while the highest dose did not accomplish additional effect) on branching and cellular proliferation. IL-6 enhanced p38-MAPK phosphorylation without changing MEK1/2 and JNK pathways. The present study suggests a physiological role for IL-6 on pulmonary branching mechanisms most likely involving p38-MAPK intracellular signalling pathway.
TypeArticle
URIhttp://hdl.handle.net/1822/67937
DOI10.1203/01.pdr.0000242300.09427.3b
ISSN0031-3998
e-ISSN1530-0447
Publisher versionhttps://www.nature.com/articles/pr2006343
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

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