title: Insulinlike growth factor I gene expression is increased in the fetal lung after tracheal ligation.
abstract: OBJECTIVE
  The mortality and morbidity in congenital diaphragmatic hernia are mainly caused by pulmonary hypoplasia. To improve clinical results, further methods inducing lung growth may have to be used. The aim of this report was to evaluate the expression of insulinlike growth factor I (IGF-I), estrogen receptor alpha, estrogen receptor beta, growth hormone receptor, and thioredoxin in a rat model of hypoplastic, hyperplastic, and normal fetal lungs to improve understanding of lung growth.
  
  
  METHODS
  Hypoplastic diaphragmatic hernia lungs were created by giving nitrofen by gavage to pregnant rats on day 9.5. Hyperplastic lungs were achieved by intrauterine tracheal ligation of rat fetuses on day 19. All lungs were harvested on gestational day 21. Total nucleic acids were extracted by proteinase K digestion and extraction in phenol/chloroform. The total nucleic acids mixture was hybridized with radioactively labeled RNA probes, and the radioactivity of the hybrids was compared with the respective standard curve of known amounts of in vitro synthesized mRNA. Immunohistochemistry staining was performed for IGF-I.
  
  
  RESULTS
  The IGF-I mRNA was significantly (P < .01) higher in hyperplastic lungs compared with control and hypoplastic lungs. The latter 2 did not differ. No difference was found between the other mRNA levels in the study groups.
  
  
  CONCLUSIONS
  IGF-I is involved in the accelerated lung growth seen after intrauterine tracheal ligation.
authors.affiliation: Division of Pediatric Surgery, Astrid Lindgren Children's Hospital, Q3:03, SE-171 76, Sweden. bjorn.frenckner@karolinska.se
authors.forename: Björn
authors.initials: B
authors.lastname: Frenckner
authors.forename: Ann-Christine
authors.initials: AC
authors.lastname: Eklöf
authors.forename: Håkan
authors.initials: H
authors.lastname: Eriksson
authors.forename: Britt
authors.initials: B
authors.lastname: Masironi
authors.forename: Lena
authors.initials: L
authors.lastname: Sahlin
mesh_terms: D000014:Abnormalities, Drug-Induced / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D047628:Estrogen Receptor alpha / Q000096:biosynthesis / Q000235:genetics; D047629:Estrogen Receptor beta / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D005326:Fetal Proteins / Q000096:biosynthesis* / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D005865:Gestational Age; D006548:Hernia, Diaphragmatic / Q000196:embryology* / Q000235:genetics / Q000378:metabolism; D006965:Hyperplasia; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis* / Q000235:genetics; D008026:Ligation; D008168:Lung / Q000002:abnormalities / Q000196:embryology* / Q000378:metabolism / Q000473:pathology; D010647:Phenyl Ethers / Q000633:toxicity; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011986:Receptors, Somatotropin / Q000096:biosynthesis / Q000235:genetics; D013879:Thioredoxins / Q000096:biosynthesis / Q000235:genetics; D014132:Trachea / Q000196:embryology* / Q000601:surgery
chemical_list: D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005326:Fetal Proteins; D010647:Phenyl Ethers; D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D013879:Thioredoxins; D007334:Insulin-Like Growth Factor I; C007350:nitrofen