title: [Changes of MAPK and Akt signaling pathways in hearts and placentas of aborted fetuses with congenital heart disease].
abstract: OBJECTIVE
  To study the changes of MAPK and Akt signaling pathways in hearts and placentas of aborted fetuses with congenital heart disease (CHD), and investigate their roles in the pathogenesis of CHD.
  
  
  METHODS
  Ten aborted fetuses with severe CHD (CHD group) and 7 gestational age-matched non-cardiac malformation aborted fetuses (control group) were enrolled. Western blot analysis was undertaken to assess the expression of p38, p38alpha, p-p38, MEF2, ERK, p-ERK, Akt, p-Akt(Ser473) and p-Akt(Thr308) in left ventricles and placentas of the fetuses, while semi-quantitative reverse transcription polymerase chain reaction analysis was used to detect the expression of p38alpha isoforms mRNA in hearts.
  
  
  RESULTS
  Compared with the heart samples of the control group, the protein expression levels of p38 and its alpha isoform in 4 cases, p-p38 in 6 cases, MEF2 in 2 cases, p-ERK in 8 cases, Akt in 4 cases, p-Akt(Ser473) and p-Akt(Thr308) in 8 cases decreased, while the protein expression levels of p-p38 in 2 cases and p-Akt(Thr308) in 1 case increased. P-p38 protein level in 3 cases and p-ERK protein level in 2 cases decreased in placentas compared with the control group. The changes of protein expression of MAPK and Akt signaling pathway in hearts were not consistent with those in placentas in the CHD group. The expression of p38alpha isoform2 mRNA showed descent tendency in 4 heart samples with CHD, while the expression of other three p38alpha isoforms mRNA was reduced in only 1 sample compared with the control group.
  
  
  CONCLUSIONS
  Dysfunction of MAPK and Akt signaling pathways is tissue-specific in aborted fetuses with CHD. The perturbed two signaling pathways in hearts may contribute to the pathogenesis of human CHD.
authors.affiliation: Department of Obstetrics and Gynecology, Nanjing University Medical School, Nanjing, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Xu
authors.forename: Zhong-Zhou
authors.initials: ZZ
authors.lastname: Yang
authors.forename: Shu
authors.initials: S
authors.lastname: Zhang
authors.forename: Shao-Gen
authors.initials: SG
authors.lastname: Wu
authors.forename: Ya-Li
authors.initials: YL
authors.lastname: Hu
mesh_terms: D005260:Female; D005333:Fetus / Q000378:metabolism*; D006330:Heart Defects, Congenital / Q000378:metabolism*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology
chemical_list: D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D048051:p38 Mitogen-Activated Protein Kinases