当前位置： SCI文献检索 > JOURNAL OF PEDIATRIC SURGERY期刊下所有文献 > Fibroblast growth factor signaling in the developing tracheoesophageal fistula.

Fibroblast growth factor signaling in the developing tracheoesophageal fistula.

Abstract：

BACKGROUND/PURPOSE:The Adriamycin-induced rat model of esophageal atresia and tracheoesophageal fistula (EA/TEF) provides a reliable system for the study of EA/TEF pathogenesis. The authors previously hypothesized that faulty branching lung morphogenesis pathways were a critical component of its pathogenesis. The authors have found evidence for faulty fibroblast growth factor (FGF) signaling related to epithelial-mesenchymal interactions in the fistula tract. To better define FGF signaling, the differential expression of FGF ligands and their receptors between lung, fistula tract, and esophagus are described. METHODS:Time-dated pregnant, Sprague-Dawley rats were injected with Adriamycin (2 mg/kg intraperitoneally) on days 6 through 9 of gestation. Tissues were processed for histology and reverse transcriptase polymerase chain reaction. FGF-1, -7 and -10 were measured from whole lung, fistula tract, and esophagus of TEF or normal embryos. Expression of FGF2RIIIb and FGF2RIIIc receptors was measured in isolated epithelium and mesenchyme of lung and fistula tract of TEF embryos as well as lung and esophagus from normal controls. RESULTS:FGF-1 mRNA was present in the fistula tract and normal and Adriamycin-exposed lung but absent from whole esophagus. Interestingly, FGF-7 mRNA was present only in normal lung. FGF-10 was present in all tissues examined. FGF2RIIIb mRNA was absent in fistula mesenchyme but present in all other tissues examined. However, the splice variant FGF2RIIIc mRNA was present in all tissues examined. CONCLUSIONS:These findings support defective FGF signaling in the rat model of EA/TEF. Absence of FGF-7 mRNA in Adriamycin-exposed tissues suggests the primary effect of Adriamycin may be to inhibit FGF-7 expression. Moreover, absence of FGF2RIIIb in fistula mesenchyme may be caused by loss of positive feedback from FGF-7, its normal obligate ligand. Understanding these specific defects in FGF signaling may provide insight into faulty mechanisms of EA/TEF.

journal_name

J Pediatr Surg

journal_title

Journal of pediatric surgery

authors

Spilde TL,Bhatia AM,Marosky JK,Preuett B,Kobayashi H,Hembree MJ,Prasadan K,Daume E,Snyder CL,Gittes GK

doi

10.1053/jpsu.2003.50082

subject

Has Abstract

pub_date

2003-03-01 00:00:00

pages

474-7; discussion 474-7

issue

eissn

0022-3468

issn

1531-5037

pii

S0022346802630908

journal_volume

pub_type

杂志文章

在线工具

Fibroblast growth factor signaling in the developing tracheoesophageal fistula.