title: Antenatal glucocorticoid therapy increase cardiac alpha-enolase levels in fetus and neonate rats.
abstract: OBJECTIVE
  Antenatal glucocorticoid therapy has been shown to prevent acute diseases including infant respiratory distress syndrome and reduce mortality, although little is known about the effects on cardiac function-related proteins in the fetus or neonate. We investigated whether cardiac function-related proteins were altered in cardiac tissues of fetuses and neonates born to pregnant rats treated by glucocorticoid.
  
  
  METHODS
  Dexamethasone (DEX) was administered to pregnant rats for 2 days on day 17 and 18 or day 19 and 20 of gestation to simulate antenatal DEX therapy, and cardiac tissues of 19- and 21-day fetuses and 1-, 3-, and 5-day neonates were analyzed using a proteomic technique with liquid chromatography-mass spectrometry/mass spectrometry.
  
  
  RESULTS
  The identified five proteins; alpha-enolase, creatine kinase-M type, beta-tubulin, troponin T, and ATP synthase beta-chain, were significantly increased in fetal cardiac tissues with DEX administration. We observed that significant increase of alpha-enolase in the 19-day fetuses by DEX using Western blotting and immunohistochemistry. ATP and cAMP levels were also increased in the fetal heart tissue. In addition, pyruvate levels were significantly increased in the fetus groups by DEX.
  
  
  CONCLUSIONS
  These results suggest that increased alpha-enolase may contribute to acceleration of glycolysis in the preterm heart.
authors: Department of Pharmacology, St. Marianna University School of Medicine 2-16-1 Sugao, Kawasaki, Kanagawa, Japan. yoshimitsu@marianna-u.ac.jp
authors: Yoshimitsu
authors: Y
authors: Tsuzuki
authors: Yuko
authors: Y
authors: Takeba
authors: Toshio
authors: T
authors: Kumai
authors: Naoki
authors: N
authors: Matsumoto
authors: Masanori
authors: M
authors: Mizuno
authors: Kotaro
authors: K
authors: Murano
authors: Kentaro
authors: K
authors: Asoh
authors: Masayuki
authors: M
authors: Takagi
authors: Hitoshi
authors: H
authors: Yamamoto
authors: Shinichi
authors: S
authors: Kobayashi
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D000242:Cyclic AMP / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000378:metabolism; D005865:Gestational Age; D005938:Glucocorticoids / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000196:embryology / Q000502:physiology; D008297:Male; D008431:Maternal-Fetal Exchange; D009206:Myocardium / Q000378:metabolism*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism*; D011247:Pregnancy; D011270:Pregnancy, Animal; D040901:Proteomics; D019289:Pyruvic Acid / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005938:Glucocorticoids; D003907:Dexamethasone; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D010751:Phosphopyruvate Hydratase