PMID- 24487124
OWN - NLM
STAT- MEDLINE
DCOM- 20140502
LR  - 20161125
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 226
IP  - 1
DP  - 2014 Apr 7
TI  - Potential role of HSP90 in mediating the interactions between estrogen receptor 
      (ER) and aryl hydrocarbon receptor (AhR) signaling pathways.
PG  - 6-13
LID - S0378-4274(14)00052-6 [pii]
LID - 10.1016/j.toxlet.2014.01.032 [doi]
AB  - The estrogen receptor (ER) and aryl hydrocarbon receptor (AhR) are 
      ligand-activated transcription factors involved in estrogen or xenobiotic 
      exposure, whereas the 90-kDa heat shock protein (HSP90), which is a ubiquitously 
      expressed molecular chaperone, is involved in the signal transduction process. 
      Although the interactions between these pathways have been under investigation, 
      the mechanisms are unclear and the potential role of HSP90 in these interactions 
      has not been reported. The results of goldfish primary hepatocytes showed that 
      exposure to PCB77 and 17beta-estradiol (E2) alone induced significant protein 
      expression of cytochrome P450 1A (CYP1A) and vitellogenin (VTG), respectively. On 
      the other hand, the combined exposure to PCB77 and E2 led to the reduction of 
      CYP1A and VTG compared to the single treatments. Although the AhRs and ERs were 
      naturally induced during the co-treatment, the total amount of HSP90 binding to 
      the receptors was not changed. Furthermore, while the HSP90 chaperon activity was 
      blocked by the specific inhibitor (geldanamycin), reciprocal inhibition between 
      AhR and ER pathways was not observed. These findings indicate a potential role of 
      HSP90 where competition between AhR and ER for binding to HSP90 can occur and 
      cause reciprocal inhibition.
CI  - Copyright (c) 2014 Elsevier Ireland Ltd. All rights reserved.
FAU - Chang, Ziwei
AU  - Chang Z
AD  - Department of Chemistry and Chemistry Institute of Functional Materials, Pusan 
      National University, Busan 609-735, Republic of Korea.
FAU - Lu, Ming
AU  - Lu M
AD  - Department of Chemistry and Chemistry Institute of Functional Materials, Pusan 
      National University, Busan 609-735, Republic of Korea.
FAU - Kim, So-Sun
AU  - Kim SS
AD  - Department of Chemistry and Chemistry Institute of Functional Materials, Pusan 
      National University, Busan 609-735, Republic of Korea.
FAU - Park, Jang-Su
AU  - Park JS
AD  - Department of Chemistry and Chemistry Institute of Functional Materials, Pusan 
      National University, Busan 609-735, Republic of Korea. Electronic address: 
      jaspark@pusan.ac.kr.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140131
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Fish Proteins)
RN  - 0 (HSP90 Heat-Shock Proteins)
RN  - 0 (Ligands)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Vitellogenins)
RN  - 0 (Water Pollutants, Chemical)
RN  - 4TI98Z838E (Estradiol)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - J6K4F9V3BA (Cadmium Chloride)
RN  - Y2I6546TMI (3,4,3',4'-tetrachlorobiphenyl)
SB  - IM
MH  - Animals
MH  - Binding, Competitive
MH  - Cadmium Chloride/toxicity
MH  - Cells, Cultured
MH  - Cytochrome P-450 CYP1A1/biosynthesis
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Induction
MH  - Estradiol/toxicity
MH  - Fish Proteins/agonists/*metabolism
MH  - Goldfish
MH  - HSP90 Heat-Shock Proteins/*metabolism
MH  - Hepatocytes/*metabolism
MH  - Ligands
MH  - Male
MH  - Polychlorinated Biphenyls/toxicity
MH  - *Receptor Cross-Talk/drug effects
MH  - Receptors, Aryl Hydrocarbon/agonists/*metabolism
MH  - Receptors, Estrogen/agonists/*metabolism
MH  - *Signal Transduction/drug effects
MH  - Up-Regulation
MH  - Vitellogenins/metabolism
MH  - Water Pollutants, Chemical/toxicity
OTO - NOTNLM
OT  - CYP1A
OT  - Goldfish
OT  - Heat shock protein 90
OT  - Primary culture
OT  - Vitellogenin
EDAT- 2014/02/04 06:00
MHDA- 2014/05/03 06:00
CRDT- 2014/02/04 06:00
PHST- 2013/12/05 00:00 [received]
PHST- 2014/01/22 00:00 [revised]
PHST- 2014/01/23 00:00 [accepted]
PHST- 2014/02/04 06:00 [entrez]
PHST- 2014/02/04 06:00 [pubmed]
PHST- 2014/05/03 06:00 [medline]
AID - S0378-4274(14)00052-6 [pii]
AID - 10.1016/j.toxlet.2014.01.032 [doi]
PST - ppublish
SO  - Toxicol Lett. 2014 Apr 7;226(1):6-13. doi: 10.1016/j.toxlet.2014.01.032. Epub 
      2014 Jan 31.