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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 1. HDAC inhibition disrupts p65-mediated repression of Bnip3 gene transcription. Panel A, Postnatal ventricular myocytes were transfected with...Show More

  Figure 1. HDAC inhibition disrupts p65-mediated repression of Bnip3 gene transcription. Panel A, Postnatal ventricular myocytes were transfected with a Bnip3 luciferase reporter with and without a p65 NF-κB expression vector in the presence and absence of trichostatin A (TSA, 10 nM). Panel B, IKKβ-mediated NF-κB activation represses Bnip3 gene transcription in ventricular myocytes. Postnatal ventricular myocytes were infected with adenoviruses encoding IKKβ (IKKβ) in the presence and absence TSA (10 nM). Endogenous Bnip3 in ventricular myocytes was examined by semiquantitative RT-PCR. Data were normalized to house keeping control gene L32. Control cells (CNTL) were transfected with the eukaryotic expression vector pcDNA3 (panel A) or infected with control adenovirus (panel B). Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested, *=statistically different from CNTL; ‡=statistically different from p65; N.S.=not significant.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 2. Interaction of p65NF-κB with HDAC1 in ventricular myocytes. Panel A, upper, Western blot analysis (WB) of cells were transfected with Flag-T...Show More

  Figure 2. Interaction of p65NF-κB with HDAC1 in ventricular myocytes. Panel A, upper, Western blot analysis (WB) of cells were transfected with Flag-Tagged p65NF-κB and immunoprecipitated (IP) with an antibody directed Flag (αFLAG). The filter was probed with anti-body directed against p65 to verify the expression of p65NF-κB. Lower panel, Western Blot analysis of total cell lysate for p65. Panel B, upper, Western Blot analysis of cell lysate from panel A immunoprecipitated with anti-Flag antibody, the filter was probed with a murine antibody directed against HDAC1. Lower panel, Western Blot analysis of total cell lysate for HDAC1.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 3. Regulation of Bnip3 gene transcription by HDAC1. Panel A, BNIP3 gene transcription in the presence of WT HDAC1 and catalytically inactive HD...Show More

  Figure 3. Regulation of Bnip3 gene transcription by HDAC1. Panel A, BNIP3 gene transcription in the presence of WT HDAC1 and catalytically inactive HDAC1 mutant (HDAC1H141A). Panel B, Regulation of Bnip3 gene transcription by p65 NF-κB in the presence and absence of WT HDAC1 and mutant HDAC1H141A. Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested, *=statistically different from CNTL; †=statistically different from HDAC1; # = statistically different from p65+HDAC1.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 4. HDAC1 mediated repression of Bnip3 gene transcription requires the DNA binding properties of NF-κB. Panel A, Regulation of Bnip3 gene transc...Show More

  Figure 4. HDAC1 mediated repression of Bnip3 gene transcription requires the DNA binding properties of NF-κB. Panel A, Regulation of Bnip3 gene transcription by HDAC1 in the presence and absence of WT p65 NF-κB designated (p65) and mutations of p65 NF-κB defective for transactivation designated (p65S529A, p65S536A) or mutations of p65NF-κB defective for DNA binding designated (p65-DB). Control cells (CNTL) were transfected with the eukaryotic expression vector pcDNA3. Panel B, Western blot (WB) analysis of cells transfected with either Flag-tagged p65 NF-κB, p65S529A, or p65S536A and immunoprecipitated (IP) with a murine antibody directed against Flag epitope (αFLAG). The filter was probed for HDAC1 (upper) and p65 (lower). Panel C, Western Blot analysis of total cell lysate from conditions shown in panel B, probed for HDAC1. Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested, *=statistically different from CNTL; †=statistically different from HDAC1; # = statistically different from p65+HDAC1, N.S.=not significant.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 5. NF-κB elements are required for repression of BNIP3 expression. Schematic of the BNIP3 promoter depicting the NF-κB response elements (NRE)...Show More

  Figure 5. NF-κB elements are required for repression of BNIP3 expression. Schematic of the BNIP3 promoter depicting the NF-κB response elements (NRE) base pairs (-1075/-1069). Postnatal ventricular myocytes were transfected with luciferase reporter plasmids containing WTBnip3 promoter (BNIP3 WT) or mutant Bnip3 promoter, in which the NF-κB elements were deleted and designated (Bnip3 mt), in the presence and absence of p65NF-κB and HDAC1. Data are expressed as mean ± S.E. fold decrease from their respective controls (BNIP3 WT or Bnip3 mt). Experiments were repeated at least n=4 with independent culture conditions using replicates of n=3 for each condition, *=statistically different from Bnip3 wt +p65NFκB; ‡=statistically different from Bnip3WT +HDAC1. Legend; ▪=Bnip3 WT; □=Bnip3mt.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 6. Bnip3 gene expression in WT and p65 deficient cells. Panel A, WT and p65−/− MEF cells23 were transfected with a BNIP3 Luciferase reporter pl...Show More

  Figure 6. Bnip3 gene expression in WT and p65 deficient cells. Panel A, WT and p65−/− MEF cells23 were transfected with a BNIP3 Luciferase reporter plasmid, in the presence and absence of HDAC1 and p65. A 3.0-fold (P<0.001) increase in basal BNIP3 gene expression was observed in p65−/− cells compared with WT cells (CNTL). Bnip3 transcription is repressed by HDAC1 in p65 +/+ cells but not in p65−/− cells. Repletion of p65 NF-κB into p65 −/− cells restored HDAC1 mediated repression of Bnip3 gene transcription. Panel B, Semiquantitative RT-PCR analysis of endogenous Bnip3 gene transcription in WT and p65 −/− MEF cells. Data are normalized to L32 expression. Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested; *=statistically different from WT CNTL; ‡=statistically different from CNTL p65 −/− cells; †=statistically different from WT CNTL with HDAC1; N.S.=not significant. Legend; ▪=WT p65+/+; □=p65−/− cells.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 7. HDAC1 activity and Bnip3 expression during hypoxia. Panel A, Normoxic control cells (CNTL) or cells subjected to hypoxia (HYPX) in the prese...Show More

  Figure 7. HDAC1 activity and Bnip3 expression during hypoxia. Panel A, Normoxic control cells (CNTL) or cells subjected to hypoxia (HYPX) in the presence and absence of TSA (10 nM) were assessed for HDAC activity. HDAC1 activity was monitored by following the deacetylation of recombinant fluormetric HDAC substrate HOS341 and is expressed as μmol/min/μg protein; control cells=1.01×10−6 μmol/min/μg protein; cells treated with TSA=6.42×10−7 μmol/min/μg protein; cells subjected to hypoxia=7.91×10−7 μmol/min/μg protein; cells treated with TSA and subjected to hypoxia=5.70×10−7μmol/min/μg protein. Data are presented as percent change from control using n=3 independent experiments and replicates of at least n=3 for each condition tested. Panel B, Bnip3 transcription during hypoxia; Bnip3 gene transcription is increased by 5.0-fold (P<0.001) in cells subjected to hypoxia compared with normoxic control cells; hypoxia-induced Bnip3 gene activation is repressed by WT HDAC1 but not the catalytically inactive mutant HDACH141A; Panels A and B, *=statistically different from normoxic control cells (CNTL); ‡=statistically different from HYPX, N.S.=not significant. Panel C, The NF-κB element is required for suppression of Bnip3 transcription by HDAC1 during hypoxia; Postnatal ventricular myocytes were transfected with luciferase reporter plasmids containing WT BNIP3 promoter (BNIP3 WT) or mutant Bnip3 promoter in which the NF-κB site was deleted and designated (Bnip3 mt) as detailed in Figure 4; *=statistically different from Bnip3 WT normoxic control; ‡=statistically different Bnip3 WT HYPX; †=statistically different from Bnip3 WT HYPX+HDAC1; #=statistically different from Bnip3 mt normoxic control. Legend ▪=Bnip3 WT; □=Bnip3 mt.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 1. HDAC inhibition disrupts p65-mediated repression of Bnip3 gene transcription. Panel A, Postnatal ventricular myocytes were transfected with...Show More

  Figure 1. HDAC inhibition disrupts p65-mediated repression of Bnip3 gene transcription. Panel A, Postnatal ventricular myocytes were transfected with a Bnip3 luciferase reporter with and without a p65 NF-κB expression vector in the presence and absence of trichostatin A (TSA, 10 nM). Panel B, IKKβ-mediated NF-κB activation represses Bnip3 gene transcription in ventricular myocytes. Postnatal ventricular myocytes were infected with adenoviruses encoding IKKβ (IKKβ) in the presence and absence TSA (10 nM). Endogenous Bnip3 in ventricular myocytes was examined by semiquantitative RT-PCR. Data were normalized to house keeping control gene L32. Control cells (CNTL) were transfected with the eukaryotic expression vector pcDNA3 (panel A) or infected with control adenovirus (panel B). Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested, *=statistically different from CNTL; ‡=statistically different from p65; N.S.=not significant.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 2. Interaction of p65NF-κB with HDAC1 in ventricular myocytes. Panel A, upper, Western blot analysis (WB) of cells were transfected with Flag-T...Show More

  Figure 2. Interaction of p65NF-κB with HDAC1 in ventricular myocytes. Panel A, upper, Western blot analysis (WB) of cells were transfected with Flag-Tagged p65NF-κB and immunoprecipitated (IP) with an antibody directed Flag (αFLAG). The filter was probed with anti-body directed against p65 to verify the expression of p65NF-κB. Lower panel, Western Blot analysis of total cell lysate for p65. Panel B, upper, Western Blot analysis of cell lysate from panel A immunoprecipitated with anti-Flag antibody, the filter was probed with a murine antibody directed against HDAC1. Lower panel, Western Blot analysis of total cell lysate for HDAC1.Show Less
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  Transcriptional Silencing of the Death Gene BNIP3 by Cooperative Action of NF-κB and Histone Deacetylase 1 in Ventricular Myocytes

  James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie, Lorrie A. Kirshenbaum

  Circulation Research December 2006, 99 (12) 1347-1354; DOI: https://doi.org/10.1161/01.RES.0000251744.06138.50

  

  By James Shaw, Tong Zhang, Marek Rzeszutek, Natalia Yurkova, Delphine Baetz, James R. Davie and Lorrie A. Kirshenbaum

  Figure 3. Regulation of Bnip3 gene transcription by HDAC1. Panel A, BNIP3 gene transcription in the presence of WT HDAC1 and catalytically inactive HD...Show More

  Figure 3. Regulation of Bnip3 gene transcription by HDAC1. Panel A, BNIP3 gene transcription in the presence of WT HDAC1 and catalytically inactive HDAC1 mutant (HDAC1H141A). Panel B, Regulation of Bnip3 gene transcription by p65 NF-κB in the presence and absence of WT HDAC1 and mutant HDAC1H141A. Data are expressed as mean ± S.E. (P<0.05). Experiments were repeated at least n=6 with independent culture conditions using replicates of n=3 for each condition tested, *=statistically different from CNTL; †=statistically different from HDAC1; # = statistically different from p65+HDAC1.Show Less

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