title: Antenatal glucocorticoid therapy accelerates ATP production with creatine kinase increase in the growth-enhanced fetal rat heart.
abstract: BACKGROUND
  Previous study has demonstrated the increase of several cardiac function-related proteins, including creatine kinase (CK) as an important enzyme in the process of ATP synthesis in the fetal heart of rats administered glucocorticoid (GC) antenatally. In the present study the effect of antenatal GC administration on the CK expression in fetal and neonatal hearts was demonstrated.
  
  
  RESULTS
  Dexamethasone was administered to pregnant rats on days 19 and 20 of gestation. The mRNA levels of the CK isoforms, CK-M and Mi-CK, in 21-day-old fetal and 1-day-old neonatal hearts were significantly increased after antenatal GC administration. CK protein levels were also increased in both cultured cardiomyocytes and the mitochondria of the hearts. Uptake of 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetraethyl-benzimidazolocarbocyanine iodide by mitochondria was significantly increased. An increased ATP level accompanied the CK increase in the neonatal hearts. Furthermore, in vitro these effects were mediated though the GC receptor of cardiomyocytes. Peroxisome proliferator-activated receptor gamma as the upstream transcription factor of CK was significantly increased in fetal hearts.
  
  
  CONCLUSIONS
  These results suggest that antenatal GC administration accelerates ATP synthesis through increased CK and may contribute to maturation of the premature heart so that it is ready for preterm delivery. (Circ J 2010; 74: 171 - 180).
authors: Department of Pediatrics, St Marianna University School of Medicine, Japan. m2.water-field@marianna-u.ac.jp
authors: Masanori
authors: M
authors: Mizuno
authors: Yuko
authors: Y
authors: Takeba
authors: Naoki
authors: N
authors: Matsumoto
authors: Yoshimitsu
authors: Y
authors: Tsuzuki
authors: Kentaro
authors: K
authors: Asoh
authors: Masayuki
authors: M
authors: Takagi
authors: Shinichi
authors: S
authors: Kobayashi
authors: Hitoshi
authors: H
authors: Yamamoto
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D052279:Creatine Kinase, MB Form / Q000378:metabolism*; D003907:Dexamethasone / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D047109:Fetal Development / Q000187:drug effects*; D005938:Glucocorticoids / Q000008:administration & dosage / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000196:embryology*; D015735:Mifepristone / Q000494:pharmacology; D023421:Models, Animal; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D047495:PPAR gamma / Q000378:metabolism; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors
chemical_list: D005938:Glucocorticoids; D047495:PPAR gamma; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D003907:Dexamethasone; D000255:Adenosine Triphosphate; D052279:Creatine Kinase, MB Form