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Bach1 Represses Wnt/ß-Catenin Signaling and Angiogenesis.
Jiang, Li; Yin, Meng; Wei, Xiangxiang; Liu, Junxu; Wang, Xinhong; Niu, Cong; Kang, Xueling; Xu, Jie; Zhou, Zhongwei; Sun, Shaoyang; Wang, Xu; Zheng, Xiaojun; Duan, Shengzhong; Yao, Kang; Qian, Ruizhe; Sun, Ning; Chen, Alex; Wang, Rui; Zhang, Jianyi; Chen, Sifeng; Meng, Dan.
Afiliação
  • Jiang L; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Yin M; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Wei X; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Liu J; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Wang X; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Niu C; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Kang X; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Xu J; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Zhou Z; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Sun S; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Wang X; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Zheng X; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Duan S; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Yao K; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Qian R; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Sun N; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Chen A; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Wang R; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Zhang J; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Chen S; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
  • Meng D; Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of
Circ Res ; 117(4): 364-375, 2015 Jul 31.
Article em En | MEDLINE | ID: mdl-26123998
ABSTRACT
RATIONALE Wnt/ß-catenin signaling has an important role in the angiogenic activity of endothelial cells (ECs). Bach1 is a transcription factor and is expressed in ECs, but whether Bach1 regulates angiogenesis is unknown.

OBJECTIVE:

This study evaluated the role of Bach1 in angiogenesis and Wnt/ß-catenin signaling. METHODS AND

RESULTS:

Hind-limb ischemia was surgically induced in Bach1(-/-) mice and their wild-type littermates and in C57BL/6J mice treated with adenoviruses coding for Bach1 or GFP. Lack of Bach1 expression was associated with significant increases in perfusion and vascular density and in the expression of proangiogenic cytokines in the ischemic hindlimb of mice, with enhancement of the angiogenic activity of ECs (eg, tube formation, migration, and proliferation). Bach1 overexpression impaired angiogenesis in mice with hind-limb ischemia and inhibited Wnt3a-stimulated angiogenic response and the expression of Wnt/ß-catenin target genes, such as interleukin-8 and vascular endothelial growth factor, in human umbilical vein ECs. Interleukin-8 and vascular endothelial growth factor were responsible for the antiangiogenic response of Bach1. Immunoprecipitation and GST pull-down assessments indicated that Bach1 binds directly to TCF4 and reduces the interaction of ß-catenin with TCF4. Bach1 overexpression reduces the interaction between p300/CBP and ß-catenin, as well as ß-catenin acetylation, and chromatin immunoprecipitation experiments confirmed that Bach1 occupies the TCF4-binding site of the interleukin-8 promoter and recruits histone deacetylase 1 to the interleukin-8 promoter in human umbilical vein ECs.

CONCLUSIONS:

Bach1 suppresses angiogenesis after ischemic injury and impairs Wnt/ß-catenin signaling by disrupting the interaction between ß-catenin and TCF4 and by recruiting histone deacetylase 1 to the promoter of TCF4-targeted genes.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Músculo Esquelético / Neovascularização Fisiológica / Células Endoteliais / Beta Catenina / Fatores de Transcrição de Zíper de Leucina Básica / Proteínas de Grupos de Complementação da Anemia de Fanconi / Via de Sinalização Wnt / Isquemia Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2015 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Músculo Esquelético / Neovascularização Fisiológica / Células Endoteliais / Beta Catenina / Fatores de Transcrição de Zíper de Leucina Básica / Proteínas de Grupos de Complementação da Anemia de Fanconi / Via de Sinalização Wnt / Isquemia Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2015 Tipo de documento: Article