Anti-inflammatory Effect of a Cell-Penetrating Peptide Targeting the Nrf2/Keap1 Interaction

被引:93
作者
Steel, Richard [1 ]
Cowan, Jonathan [1 ]
Payerne, Estelle [1 ]
O'Connell, Maria A. [1 ]
Searcey, Mark [1 ]
机构
[1] Univ E Anglia, Sch Pharm, Norwich NR4 7TJ, Norfolk, England
基金
英国工程与自然科学研究理事会;
关键词
cell-penetrating peptide; Nrf2; Keap-1; protein-protein interaction; inflammation; antioxidant response; ANTIOXIDANT RESPONSE ELEMENT; TRANSCRIPTION FACTOR NRF2; CYTOPROTECTIVE GENES; ENZYME GENES; EXPRESSION; INDUCTION; PATHWAY; PROTEIN; DELIVERY; MOUSE;
D O I
10.1021/ml300041g
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is increasingly recognized as a central regulator of multiple signaling pathways in inflammation and cancer, and the ability to use chemical biological tools to investigate its biological effects is very attractive. A peptide comprising a TAT-conjugated Nrf2 sequence is shown to activate Nrf2 and its downstream target gene heme-oxygenase-1 (HO-1) in a dose-dependent manner in intact human THP-1 monocytes. Levels of Nrf2 protein peak after 3 h, whereas HO-1 mRNA and protein peak after 6 and 12 h, respectively. The peptide is also shown to inhibit the production of the pro-inflammatory cytokine TNF. The TAT-14mer constitutes a useful chemical biology tool with potential therapeutic applications.
引用
收藏
页码:407 / 410
页数:4
相关论文
共 20 条
[1]   Nrf2, a Cap'n'Collar transcription factor, regulates induction of the heme oxygenase-1 gene [J].
Alam, J ;
Stewart, D ;
Touchard, C ;
Boinapally, S ;
Choi, AMK ;
Cook, JL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (37) :26071-26078
[2]   Impaired expression of glutathione synthetic enzyme genes in mice with targeted deletion of the Nrf2 basic-leucine zipper protein [J].
Chan, JY ;
Kwong, M .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 2000, 1517 (01) :19-26
[3]   Induction of cytoprotective genes through Nrf2/antioxidant response element pathway: A new therapeutic approach for the treatment of inflammatory diseases [J].
Chen, XL ;
Kunsch, C .
CURRENT PHARMACEUTICAL DESIGN, 2004, 10 (08) :879-891
[4]   Cell-penetrating peptides: tools for intracellular delivery of therapeutics [J].
Deshayes, S ;
Morris, MC ;
Divita, G ;
Heitz, F .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2005, 62 (16) :1839-1849
[5]   Peptide inhibitors of the Keap1-Nrf2 protein-protein interaction [J].
Hancock, Rowena ;
Bertrand, Helene C. ;
Tsujita, Tadayuki ;
Naz, Shama ;
El-Bakry, Ayman ;
Laoruchupong, Jitnueng ;
Hayes, John D. ;
Wells, Geoff .
FREE RADICAL BIOLOGY AND MEDICINE, 2012, 52 (02) :444-451
[6]   Transcription factor Nrf2 is required for the constitutive and inducible expression of multidrug resistance-associated protein 1 in mouse embryo fibroblasts [J].
Hayashi, A ;
Suzuki, H ;
Itoh, K ;
Yamamoto, M ;
Sugiyama, Y .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 310 (03) :824-829
[7]   A Small-Molecule Inducer of the Antioxidant Response Element [J].
Hur, Wooyoung ;
Sun, Zheng ;
Jiang, Tao ;
Mason, Daniel E. ;
Peters, Eric C. ;
Zhang, Donna D. ;
Luesch, Hendrik ;
Schultz, Peter G. ;
Gray, Nathanael S. .
CHEMISTRY & BIOLOGY, 2010, 17 (05) :537-547
[8]   Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain [J].
Itoh, K ;
Wakabayashi, N ;
Katoh, Y ;
Ishii, T ;
Igarashi, K ;
Engel, JD ;
Yamamoto, M .
GENES & DEVELOPMENT, 1999, 13 (01) :76-86
[9]   An Nrf2 small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements [J].
Itoh, K ;
Chiba, T ;
Takahashi, S ;
Ishii, T ;
Igarashi, K ;
Katoh, Y ;
Oyake, T ;
Hayashi, N ;
Satoh, K ;
Hatayama, I ;
Yamamoto, M ;
Nabeshima, Y .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 236 (02) :313-322
[10]   CLONING AND CHARACTERIZATION OF A NOVEL ERYTHROID CELL-DERIVED CNC FAMILY TRANSCRIPTION FACTOR HETERODIMERIZING WITH THE SMALL MAF FAMILY PROTEINS [J].
ITOH, K ;
IGARASHI, K ;
HAYASHI, N ;
NISHIZAWA, M ;
YAMAMOTO, M .
MOLECULAR AND CELLULAR BIOLOGY, 1995, 15 (08) :4184-4193