The possible role of heat shock factor-1 in the negative regulation of heme oxygenase-1

被引：22

作者：

Chou, YH

Ho, FM

Liu, DZ

Lin, SY

Tsai, LH

Chen, CH

Ho, YS

Hung, LF

Liang, YC

机构：

[1] Taipei Med Univ, Coll Med, Grad Inst Biomed Technol, Taipei 11014, Taiwan

[2] Shin Kong Wu Ho Su Mem Hosp, Dept Surg, Taipei, Taiwan

[3] Taipei Med Univ, Coll Oral Med, Grad Inst Biomed Mat, Taipei 11014, Taiwan

[4] Taipei Med Univ, Coll Med, Dept Internal Med, Taipei, Taiwan

[5] Taipei Med Univ, Coll Med, Dept Physiol, Taipei, Taiwan

[6] Tao Yuan Gen Hosp, Dept Hlth Taiwan, Taoyuan, Taiwan

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2005年 / 37卷 / 03期

关键词：

heme oxygenase-1; heat shock factor-1; hepatoma; arsenite; 15-deoxy-Delta(12,14)-prostaglandin J(2);

D O I：

10.1016/j.biocel.2004.08.006

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

We examined a possible role for heat shock factor- 1 (HSF-1) in the negative regulation of HO-1 gene expression in human Hep3Bhepatomacel Is responding to stimulation with 15-deoxy- Delta(12,14) -prostaglandin J(2) (15d-PGJ(2)) and arsenite. Overexpression of HSF- 1 and heat-shock experiments indicated that HSF- I repressed the 15d-PGJ(2)-and arsenite-induced HO- 1 gene expression through directly binding to the consensus heat shock element (HSE) of the HO-1 gene promoter. In addition, point mutations at specific HSE sequences of the HO-1 promoter-driven luciferase plasmid (pGL2/hHO3.2-Luc) abolished the heat shock- and HSF- I -mediated repression of reporter activity. Overall, it is possible that HSF- I negatively regulates HO- 1 gene expression, and that the HSE present in the -389 to -362 region mediates HSF- I -induced repression of human HO- I gene expression. (C) 2004 Elsevier Ltd. All rights reserved.

引用

页码：604 / 615

页数：12

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