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Differential Protein Expression in Heart in UT‐B Null Mice with Cardiac Conduction Defects
Author(s) -
hao Yu,
Meng yan,
Zhao lijuan,
Wang lishun,
Jin xian,
Li yang,
Chen guoqiang,
Zhao xuejian,
Yang baoxue
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.963.1
Subject(s) - western blot , genetically modified mouse , chemistry , microbiology and biotechnology
Cardiac conduction defects were found in transgenic mice deficient in UT‐B. To investigate the molecular mechanisms of the conduction defects caused by UT‐B deletion, we studied the protein expression profiles of heart tissue in UT‐B null mice vs age‐matched wild‐type mice at different developmental stages. Using two‐dimensional electrophoresis in combination with matrix‐assisted laser desorption/ionization time‐of‐flight (MALDI‐TOF‐TOF) tandem mass spectrometry, we found that 26 proteins were modulated in the myocardium of UT‐B null mice. Of the modulated proteins, troponin T, cardiac (TNNT2) was up‐regulated 5.31 ± 0.45 (n = 3) folds in 16 weeks old UT‐B null mice and down‐regulated 3.99 ± 0.40 folds in 52 weeks old mice. Atrial natriuretic peptide (ANP) was up‐regulated 4.18 ± 0.61 folds in 52 weeks old UT‐B null mice with AV block. The modulation of these 2 proteins was confirmed by the Western‐blot analysis. The results indicate that UT‐B deletion caused the expression regulation of TNNT2 and ANP in mouse heart with cardiac conduction defect, which provides new clues to the mechanism involved in cardiac conduction defect.