PMID- 10413595
OWN - NLM
STAT- MEDLINE
DCOM- 19990819
LR  - 20191210
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 250
IP  - 2
DP  - 1999 Aug 1
TI  - Comparison of chromatin remodeling and transcriptional activation of the mouse 
      mammary tumor virus promoter by the androgen and glucocorticoid receptor.
PG  - 414-22
AB  - We examined the interaction between the androgen (AR) and glucocorticoid receptor 
      (GR) at the transcriptional level using mouse fibroblast cell lines harboring an 
      integrated mouse mammary tumor virus (MMTV) promoter. We found that the AR, after 
      induction with dihydrotestosterone (DHT), caused a progressive increase in 
      MMTV-CAT reporter activity over 72 h which was correlated to an increase in 
      chromatin remodeling of the MMTV promoter in the vicinity of the hormone response 
      element (HRE). In contrast, stimulation of the GR by the synthetic glucocorticoid 
      dexamethasone (Dex) caused a transient increase in MMTV transcriptional activity 
      which returned to basal levels after 72 h. These changes were correlated to a 
      transient increase in chromatin remodeling in the region of the HRE. Neither 
      cotreatment nor pretreatment with Dex affected the DHT response. In fact, there 
      was a more than additive effect of the two hormones on transcription at early 
      time points. This suggests that the inability of GR to remodel chromatin, after 
      24 h of hormone treatment, is most likely related to changes in the GR itself and 
      not the chromatin remodeling process. Consistent with this, nuclear GR levels 
      dropped by greater than 50% after Dex treatment whereas the AR was induced 
      fourfold after 24 h of DHT treatment. We conclude that a promoter with an ordered 
      chromatin structure can still respond to androgens even after its glucocorticoid 
      responsiveness is lost. This may be one mechanism cells utilize to establish 
      target gene specificity for nuclear receptors that recognize identical DNA 
      sequences.
CI  - Copyright 1999 Academic Press.
FAU - List, H J
AU  - List HJ
AD  - Department of Pharmacology, Georgetown University, Washington, DC, 20007, USA.
FAU - Lozano, C
AU  - Lozano C
FAU - Lu, J
AU  - Lu J
FAU - Danielsen, M
AU  - Danielsen M
FAU - Wellstein, A
AU  - Wellstein A
FAU - Riegel, A T
AU  - Riegel AT
LA  - eng
GR  - DK02141/DK/NIDDK NIH HHS/United States
GR  - DK42552/DK/NIDDK NIH HHS/United States
GR  - DK43127/DK/NIDDK NIH HHS/United States
GR  - etc.
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Chromatin)
RN  - 0 (Receptors, Androgen)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 08J2K08A3Y (Dihydrotestosterone)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 3.1.21.- (endodeoxyribonuclease SacI)
RN  - EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Nucleus/drug effects/metabolism
MH  - Chromatin/chemistry/*genetics/metabolism
MH  - Deoxyribonucleases, Type II Site-Specific/metabolism
MH  - Dexamethasone/pharmacology
MH  - Dihydrotestosterone/pharmacology
MH  - Genes, Reporter
MH  - L Cells
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Molecular Structure
MH  - Promoter Regions, Genetic/*genetics
MH  - Receptors, Androgen/*metabolism
MH  - Receptors, Glucocorticoid/*metabolism
MH  - Time Factors
MH  - Transcriptional Activation/drug effects/*genetics
MH  - Transfection
EDAT- 1999/07/22 00:00
MHDA- 1999/07/22 00:01
CRDT- 1999/07/22 00:00
PHST- 1999/07/22 00:00 [pubmed]
PHST- 1999/07/22 00:01 [medline]
PHST- 1999/07/22 00:00 [entrez]
AID - S0014-4827(99)94517-2 [pii]
AID - 10.1006/excr.1999.4517 [doi]
PST - ppublish
SO  - Exp Cell Res. 1999 Aug 1;250(2):414-22. doi: 10.1006/excr.1999.4517.