PMID- 21494593
OWN - NLM
STAT- MEDLINE
DCOM- 20110816
LR  - 20211020
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 6
IP  - 4
DP  - 2011 Apr 11
TI  - Regulation of mouse small heat shock protein alphab-crystallin gene by aryl 
      hydrocarbon receptor.
PG  - e17904
LID - 10.1371/journal.pone.0017904 [doi]
LID - e17904
AB  - The stress-inducible small heat shock protein (shsp)/alphaB-crystallin gene is 
      expressed highly in the lens and moderately in other tissues. Here we provide 
      evidence that it is a target gene of the aryl hydrocarbon receptor (AhR) 
      transcription factor. A sequence (-329/-323, CATGCGA) similar to the consensus 
      xenobiotic responsive element (XRE), called here XRE-like, is present in the alphaBE2 
      region of alphaB-crystallin enhancer and can bind AhR in vitro and in vivo. 
      alphaB-crystallin protein levels were reduced in retina, lens, cornea, heart, 
      skeletal muscle and cultured muscle fibroblasts of AhR(-/-) mice; alphaB-crystallin 
      mRNA levels were reduced in the eye, heart and skeletal muscle of AhR(-/-) mice. 
      Increased AhR stimulated alphaB-crystallin expression in transfection experiments 
      conducted in conjunction with the aryl hydrocarbon receptor nuclear translocator 
      (ARNT) and decreased AhR reduced alphaB-crystallin expression. AhR effect on 
      aB-crystallin promoter activity was cell-dependent in transfection experiments. 
      AhR up-regulated alphaB-crystallin promoter activity in transfected HeLa, NIH3T3 and 
      COS-7 cells in the absence of exogenously added ligand (TCDD), but had no effect 
      on the alphaB-crystallin promoter in C(2)C(12), CV-1 or Hepa-1 cells with or without 
      TCDD. TCDD enhanced AhR-stimulated alphaB-crystallin promoter activity in transfected 
      alphaTN4 cells. AhR could bind to an XRE-like site in the alphaB-crystallin enhancer in 
      vitro and in vivo. Finally, site-specific mutagenesis experiments showed that the 
      XRE-like motif was necessary for both basal and maximal AhR-induction of 
      alphaB-crystallin promoter activity. Our data strongly suggest that AhR is a 
      regulator of alphaB-crystallin gene expression and provide new avenues of research 
      for the mechanism of tissue-specific alphaB-crystallin gene regulation under normal 
      and physiologically stressed conditions.
FAU - Liu, Shuang
AU  - Liu S
AD  - Laboratory of Molecular and Developmental Biology, National Eye Institute, 
      National Institutes of Health, Bethesda, Maryland, United States of America. 
      liushuang1999@yahoo.com
FAU - Piatigorsky, Joram
AU  - Piatigorsky J
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20110411
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Cryab protein, mouse)
RN  - 0 (DNA, Intergenic)
RN  - 0 (HSP27 Heat-Shock Proteins)
RN  - 0 (Hspb2 protein, mouse)
RN  - 0 (Ligands)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (alpha-Crystallin B Chain)
RN  - 138391-32-9 (Aryl Hydrocarbon Receptor Nuclear Translocator)
SB  - IM
MH  - Animals
MH  - Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism
MH  - Base Sequence
MH  - Binding Sites
MH  - Binding, Competitive/drug effects
MH  - DNA, Intergenic/genetics
MH  - Enhancer Elements, Genetic/genetics
MH  - *Gene Expression Regulation/drug effects
MH  - Gene Knockdown Techniques
MH  - HSP27 Heat-Shock Proteins/genetics/metabolism
MH  - HeLa Cells
MH  - Humans
MH  - Ligands
MH  - Mice
MH  - Molecular Sequence Data
MH  - Organ Specificity/drug effects
MH  - Polychlorinated Dibenzodioxins/pharmacology
MH  - Promoter Regions, Genetic/genetics
MH  - Protein Binding/drug effects
MH  - Receptors, Aryl Hydrocarbon/deficiency/*metabolism
MH  - alpha-Crystallin B Chain/*genetics/metabolism
PMC - PMC3073930
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2011/04/16 06:00
MHDA- 2011/08/17 06:00
PMCR- 2011/04/11
CRDT- 2011/04/16 06:00
PHST- 2010/08/30 00:00 [received]
PHST- 2011/02/16 00:00 [accepted]
PHST- 2011/04/16 06:00 [entrez]
PHST- 2011/04/16 06:00 [pubmed]
PHST- 2011/08/17 06:00 [medline]
PHST- 2011/04/11 00:00 [pmc-release]
AID - PONE-D-10-03188 [pii]
AID - 10.1371/journal.pone.0017904 [doi]
PST - epublish
SO  - PLoS One. 2011 Apr 11;6(4):e17904. doi: 10.1371/journal.pone.0017904.