The aryl hydrocarbon receptor (AhR) pathway as a regulatory pathway for cell adhesion and matrix metabolism

被引:74
作者
Kung, Tiffany [1 ,2 ]
Murphy, K. A. [1 ,3 ]
White, L. A. [1 ]
机构
[1] Rutgers State Univ, Dept Biochem & Microbiol, New Brunswick, NJ 08901 USA
[2] Rutgers State Univ, Joint Grad Program Toxicol, New Brunswick, NJ 08901 USA
[3] Rutgers State Univ, Joint Grad Program Biochem, New Brunswick, NJ 08901 USA
关键词
AhR; Extracellular matrix (ECM); Matrix metalloproteinase (MMP); 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); Development; NF-KAPPA-B; LACTATIONAL 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN EXPOSURE; POLYCYCLIC AROMATIC-HYDROCARBONS; MAMMARY-GLAND DIFFERENTIATION; MARMOSETS CALLITHRIX-JACCHUS; ACTIVATED PROTEIN-KINASES; LIVER EPITHELIAL-CELLS; T-CADHERIN EXPRESSION; BREAST-CANCER CELLS; GROWTH-FACTOR-BETA;
D O I
10.1016/j.bcp.2008.09.031
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The aryl hydrocarbon receptor (AhR) is an orphan receptor in the basic helix-loop-helix PAS family of transcriptional regulators. Although the endogenous regulator of this pathway has not been identified, the AhR is known to bind and be activated by a variety of compounds ranging from environmental contaminants to flavanoids. The function of this receptor is still unclear; however, animal models indicate that the AhR is important for normal development. One hypothesis is that the AhR senses cellular stress and initiates the cellular response by altering gene expression and inhibiting cell cycle progression and that activation of the AhR by exogenous environmental chemicals results in the dysregulation of this normal function. In this review we will examine the role of the AhR in the regulation of genes and proteins involved in cell adhesion and matrix remodeling, and discuss the implications of these changes in development and disease. In addition, we will discuss evidence suggesting that the AhR pathway is responsive to changes in matrix composition as well as cell-cell and cell-matrix interactions. (C) 2008 Elsevier Inc. All rights reserved
引用
收藏
页码:536 / 546
页数:11
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