Ghrelin expression in human and rat fetal lungs and the effect of ghrelin administration in nitrofen-induced congenital diaphragmatic hernia

• Type: Article in International Scientific Journal
• Date: 2006

Authors

Santos M (Author) Other; Bastos P (Author) Other; Gonzaga S (Author) Other; Roriz JM (Author) Other; Baptista MJ (Author) Other; Nogueira-Silva C (Author) Other; Melo-Rocha G (Author) Other; Henriques-Coelho T (Author) FMUP; Roncon-Albuquerque R Jr (Author) FMUP; Leite-Moreira AF (Author) FMUP; De Krijger RR (Author) Other; Tibboel D (Author) Other; Rottier R (Author) Other; Correia-Pinto J (Author) Other

Journal

Title: Pediatric Research

Vol. 59

Pages: 531-537

ISSN: 0031-3998

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 39 Citations

Scopus - 40 Citations

Pubmed / Medline

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Authenticus ID: P-004-MK4

DOI: 10.1203/01.pdr.0000202748.66359.a9

Abstract (EN): Ghrelin is a strong physiologic growth hormone secretagogue that exhibits endocrine and non-endocrine actions. In this study, ghrelin expression in humans and rats was evaluated throughout development of normal and hypoplastic lungs associated with congenital diaphragmatic hernia (CDH). Additionally, the effect of antenatal treatment with ghrelin in the nitrofen-induced CDH rat model was tested. In normal lungs, ghrelin was expressed in the primitive epithelium at early stages of development and decreased in levels of expression with gestational age. In hypoplastic lungs ghrelin was overexpressed in both human and rat CDH fetuses when compared with controls. Exogenous administration of ghrelin to nitrofentreated darns led to an attenuation of pulmonary hypoplasia of CDH pups. Furthermore, the growth hormone, secretagogue receptor (GHSR1a), could not be amplified from human or rat fetal lungs by RT-PCR. In conclusion, of all the lungs studied so far, the fetal lung is one of the first to express ghrelin during development and might be considered a new source of circulating fetal ghrelin. Overexpression of ghrelin in hypoplastic lungs and the effect of exogenous administration of ghrelin to nitrofen-treated darns strongly suggest a role for ghrelin in mechanisms involved in attenuation of fetal lung hypoplasia, most likely through a GHSR1a-independent pathway.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 7