Item request has been placed! ×
Item request cannot be made. ×
loading  Processing Request

Sodium valproate-induced congenital cardiac abnormalities in mice are associated with the inhibition of histone deacetylase.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
اقرأ على الانترنت اقرأ أكثر حفظ في قائمتي
  • المؤلفون: Wu G;Wu G; Nan C; Rollo JC; Huang X; Tian J
  • المصدر:
    Journal of biomedical science [J Biomed Sci] 2010 Mar 10; Vol. 17, pp. 16. Date of Electronic Publication: 2010 Mar 10.
  • نوع النشر :
    Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • اللغة:
    English
  • معلومة اضافية
    • المصدر:
      Publisher: BioMed Central Country of Publication: England NLM ID: 9421567 Publication Model: Electronic Cited Medium: Internet ISSN: 1423-0127 (Electronic) Linking ISSN: 10217770 NLM ISO Abbreviation: J Biomed Sci Subsets: MEDLINE
    • بيانات النشر:
      Publication: 2009- : London : BioMed Central
      Original Publication: Basel ; New York : S. Karger Medical and Scientific Publishers, c1994-
    • الموضوع:
      Anticonvulsants/*toxicity ; Heart Defects, Congenital/*chemically induced ; Histone Deacetylase Inhibitors/*toxicity ; Teratogens/*toxicity ; Valproic Acid/*toxicity; Animals ; Anticonvulsants/administration & dosage ; Female ; Histone Deacetylase 1/antagonists & inhibitors ; Histone Deacetylase 1/metabolism ; Histone Deacetylase 2/antagonists & inhibitors ; Histone Deacetylase 2/metabolism ; Histone Deacetylase Inhibitors/administration & dosage ; Histone Deacetylases/metabolism ; Mice ; Mice, Inbred C57BL ; Reverse Transcriptase Polymerase Chain Reaction ; Valproic Acid/administration & dosage
    • نبذة مختصرة :
      Background: Valproic acid, a widely used anticonvulsant drug, is a potent teratogen resulting in various congenital abnormalities. However, the mechanisms underlying valproic acid induced teratogenesis are nor clear. Recent studies indicate that histone deacetylase is a direct target of valproic acid.
      Methods: In the present study, we have used histological analysis and RT-PCR assays to examine the cardiac abnormalities in mice treated with sodium valproate (NaVP) and determined the effects of NaVP on histone deacetylase activity and the expression of heart development-related genes in mouse myocardial cells.
      Results: The experimental data show that NaVP can induce cardiac abnormalities in fetal mice in a dose-dependent manner. NaVP causes a dose-dependent inhibition of hitone deacetylase (HDAC) activity in mouse myocardial cells. However, the expression levels of HDAC (both HDAC1 and HDAC2) are not significantly changed in fetal mouse hearts after administration of NaVP in pregnant mice. The transcriptional levels of other heart development-related genes, such as CHF1, Tbx5 and MEF2, are significantly increased in fetal mouse hearts treated with NaVP.
      Conclusions: The study indicates that administration of NaVP in pregnant mice can result in various cardiac abnormalities in fetal hearts, which is associated with an inhibition of histone deacetylase without altering the transcription of this enzyme.
    • References:
      Trends Biochem Sci. 2000 Mar;25(3):121-6. (PMID: 10694882)
      Trends Pharmacol Sci. 2009 Oct;30(10):509-14. (PMID: 19762089)
      Dev Biol. 2000 Jul 1;223(1):169-80. (PMID: 10864469)
      Am J Med Genet. 2001 Jan 15;98(2):168-75. (PMID: 11223853)
      Childs Nerv Syst. 2001 Jun;17(7):399-404. (PMID: 11465793)
      EMBO J. 2001 Dec 17;20(24):6969-78. (PMID: 11742974)
      Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
      EMBO Rep. 2002 Mar;3(3):224-9. (PMID: 11882541)
      Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16197-202. (PMID: 12454287)
      Structure. 2004 Jul;12(7):1325-34. (PMID: 15242608)
      Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15064-9. (PMID: 15477595)
      Teratology. 1993 Aug;48(2):127-32. (PMID: 8211818)
      Teratog Carcinog Mutagen. 1996;16(2):97-108. (PMID: 8875740)
      Nat Genet. 1997 Jan;15(1):21-9. (PMID: 8988164)
      Nat Genet. 1997 Jan;15(1):30-5. (PMID: 8988165)
      Science. 1997 May 30;276(5317):1404-7. (PMID: 9162005)
      Nature. 1997 Sep 25;389(6649):349-52. (PMID: 9311776)
      Nature. 1998 Apr 23;392(6678):831-5. (PMID: 9572144)
      Dev Biol. 1999 Jul 1;211(1):100-8. (PMID: 10373308)
      Nature. 1999 Sep 9;401(6749):188-93. (PMID: 10490031)
      Can J Physiol Pharmacol. 2004 Oct;82(10):927-33. (PMID: 15573154)
      Tissue Cell. 2005 Feb;37(1):47-51. (PMID: 15695175)
      Prenat Diagn. 2005 Feb;25(2):156-8. (PMID: 15712340)
      Expert Opin Drug Saf. 2005 Mar;4(2):345-53. (PMID: 15794725)
      J Clin Pharm Ther. 2005 Oct;30(5):417-21. (PMID: 16164485)
      J Mol Cell Cardiol. 2006 Feb;40(2):267-73. (PMID: 16242143)
      Circulation. 2006 Jul 25;114(4):298-308. (PMID: 16847152)
      Expert Opin Pharmacother. 2008 Feb;9(2):285-92. (PMID: 18201150)
      Curr Opin Cell Biol. 2000 Jun;12(3):326-33. (PMID: 10801466)
    • Grant Information:
      S06GM-073621 United States GM NIGMS NIH HHS
    • الرقم المعرف:
      0 (Anticonvulsants)
      0 (Histone Deacetylase Inhibitors)
      0 (Teratogens)
      614OI1Z5WI (Valproic Acid)
      EC 3.5.1.98 (Histone Deacetylase 1)
      EC 3.5.1.98 (Histone Deacetylase 2)
      EC 3.5.1.98 (Histone Deacetylases)
    • الموضوع:
      Date Created: 20100312 Date Completed: 20100629 Latest Revision: 20220318
    • الموضوع:
      20221213
    • الرقم المعرف:
      PMC2841099
    • الرقم المعرف:
      10.1186/1423-0127-17-16
    • الرقم المعرف:
      20219112