PMID- 9685220
OWN - NLM
STAT- MEDLINE
DCOM- 19980925
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 138
IP  - 1-2
DP  - 1998 Mar 16
TI  - Suppression of relaxin gene expression by retinoids in squamous differentiated 
      rabbit tracheal epithelial cells.
PG  - 115-25
AB  - Northern blot analysis of total RNA from a variety of rabbit tissues indicated 
      that placenta is the primary site of expression of the protein hormone relaxin 
      (previously called SQ10) in rabbits. Relaxin was not detected by this method in 
      other rabbit tissues, including normal trachea and several squamous tissues. 
      However, relaxin is highly induced during squamous cell differentiation in 
      cultured rabbit tracheal epithelial (RbTE) cells. Retinoic acid and retinoids 
      that selectively bind to the nuclear retinoid receptors, the retinoic acid 
      receptors (RARs) and the retinoid X receptors (RXRs), and induce RARE- or 
      RXRE-dependent transactivation as well as repression of AP-1-dependent 
      transactivation, were all effective in suppressing relaxin expression. In 
      addition, the retinoid SR11302, which exhibits only anti-AP-1 activity but does 
      not induce RARE- or RXRE-dependent transactivation, was also able to inhibit 
      relaxin expression. These results suggest that the suppression of relaxin 
      expression is related to the anti-AP-1 activity of retinoids. To determine 
      whether the relaxin gene is regulated by retinoids at the level of transcription, 
      a 4.3 kb fragment of the 5' flanking region of the rabbit relaxin gene was cloned 
      and analyzed. This regulatory region included a classic TATA-box as well as 
      consensus sequences for several transcription factors, including CREB, NF-kappaB 
      and AP-1. The ability of the 4.3 kb regulatory region to control the 
      transcription of a luciferase reporter gene was analyzed in transiently 
      transfected, squamous-differentiated RbTE cells. The results demonstrated that 
      this regulatory region caused strong transactivation of the reporter gene. This 
      transactivation was inhibited by retinoic acid, suggesting retinoid control at 
      the transcriptional level. Deletion analysis indicated that multiple regulatory 
      elements are involved in the regulation of relaxin gene expression during 
      squamous differentiation as well as in the suppression by retinoids.
FAU - Bernacki, S H
AU  - Bernacki SH
AD  - Cystic Fibrosis Research and Treatment Center, School of Medicine, University of 
      North Carolina at Chapel Hill, 27599, USA.
FAU - Medvedev, A
AU  - Medvedev A
FAU - Holloway, G
AU  - Holloway G
FAU - Dawson, M
AU  - Dawson M
FAU - Lotan, R
AU  - Lotan R
FAU - Jetten, A M
AU  - Jetten AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Oligodeoxyribonucleotides)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factors)
RN  - 5688UTC01R (Tretinoin)
RN  - 9002-69-1 (Relaxin)
RN  - EC 1.13.12.- (Luciferases)
RN  - EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Chloramphenicol O-Acetyltransferase/biosynthesis/genetics
MH  - Consensus Sequence
MH  - Epithelial Cells/cytology/drug effects/*metabolism
MH  - Gene Expression Regulation/drug effects/*physiology
MH  - Genes, Reporter
MH  - Genomic Library
MH  - Luciferases/biosynthesis/genetics
MH  - Molecular Sequence Data
MH  - Oligodeoxyribonucleotides
MH  - Rabbits
MH  - Receptors, Retinoic Acid/metabolism
MH  - *Regulatory Sequences, Nucleic Acid
MH  - Relaxin/biosynthesis/*genetics
MH  - Retinoid X Receptors
MH  - Retinoids/*pharmacology
MH  - TATA Box
MH  - Trachea/cytology/drug effects/*metabolism
MH  - Transcription Factor AP-1/metabolism
MH  - Transcription Factors/metabolism
MH  - Transfection
MH  - Tretinoin/pharmacology
EDAT- 1998/07/31 00:00
MHDA- 1998/07/31 00:01
CRDT- 1998/07/31 00:00
PHST- 1998/07/31 00:00 [pubmed]
PHST- 1998/07/31 00:01 [medline]
PHST- 1998/07/31 00:00 [entrez]
AID - S0303-7207(98)00013-6 [pii]
AID - 10.1016/s0303-7207(98)00013-6 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 1998 Mar 16;138(1-2):115-25. doi: 
      10.1016/s0303-7207(98)00013-6.