PMID- 8666585
OWN - NLM
STAT- MEDLINE
DCOM- 19960806
LR  - 20190821
IS  - 0021-9290 (Print)
IS  - 0021-9290 (Linking)
VI  - 28
IP  - 12
DP  - 1995 Dec
TI  - Multiple cis-elements mediate shear stress-induced gene expression.
PG  - 1451-7
AB  - Fluid shear stress activates the expression of immediate early (IE) genes in 
      vascular endothelial cells. The transcriptional regulation can be mediated 
      through the shear stress-sensitive cis-acting elements at the 5' promoter regions 
      of various IE genes such as the monocyte chemotactic protein-1 (MCP-1) gene. We 
      linked wild-type and mutated MCP-1 promoters to the reporter gene luciferase and 
      used such constructs to investigate the role of the phorbol ester TPA responsive 
      element (TRE) in the shear-induced MCP-1 gene expression in vascular endothelial 
      cells. Functional analysis showed that TGACTCC (a divergent TRE) located at nt 
      -54 to -60 is necessary for shear-inducibility in bovine aortic endothelial cells 
      (BAEC). The induction of the wild-type MCP-1 promoter construct by shear stress 
      was attenuated by pretreating the cells with 1 microM dexamethasone or 1 microM 
      retinoic acid 12 h before the shear stress experiments. The induction by shear 
      stress reduced from 13-fold in the untreated cells to 7- and 3-folds in the 
      dexamethasone- and retinoic acid-treated cells, respectively. These results 
      demonstrate that the glucocorticoid receptor and retinoic acid receptor may 
      interfere with the shear stress-activated AP-1/TRE. The reporter activity of 
      HIV(LTR), which is a plasmid construct of the long terminal repeats of the human 
      immunodeficiency virus and contains a kappa B enhancer element, was also 
      activated by shear stress. The results of our investigations indicate that the 
      shear stress-induced IE gene expression can be mediated through multiple 
      cis-elements.
FAU - Shyy, J Y
AU  - Shyy JY
AD  - Department of Bioengineering, University of California, La Jolla 92093-0412, USA. 
      Schien@bioeng.ucsd.edu.
FAU - Li, Y S
AU  - Li YS
FAU - Lin, M C
AU  - Lin MC
FAU - Chen, W
AU  - Chen W
FAU - Yuan, S
AU  - Yuan S
FAU - Usami, S
AU  - Usami S
FAU - Chien, S
AU  - Chien S
LA  - eng
GR  - HL 19454/HL/NHLBI NIH HHS/United States
GR  - HL 43026/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biomech
JT  - Journal of biomechanics
JID - 0157375
RN  - 0 (Carcinogens)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glucocorticoids)
RN  - 0 (Keratolytic Agents)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Transcription Factor AP-1)
RN  - 5688UTC01R (Tretinoin)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 1.13.12.- (Luciferases)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Carcinogens/pharmacology
MH  - Cattle
MH  - Chemokine CCL2/genetics
MH  - Dexamethasone/pharmacology
MH  - Endothelium, Vascular/drug effects/metabolism/*physiology
MH  - Enhancer Elements, Genetic/*genetics
MH  - *Gene Expression Regulation/drug effects
MH  - Genes, Immediate-Early/drug effects/*genetics
MH  - Genes, Reporter/genetics
MH  - Genes, env/genetics
MH  - Glucocorticoids/pharmacology
MH  - Keratolytic Agents/pharmacology
MH  - Luciferases/genetics
MH  - Promoter Regions, Genetic/drug effects/genetics
MH  - Receptors, Glucocorticoid/genetics
MH  - Receptors, Retinoic Acid/genetics
MH  - Rheology
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Transcription Factor AP-1/genetics
MH  - Transcription, Genetic/drug effects
MH  - Tretinoin/pharmacology
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - 0021-9290(95)00093-3 [pii]
AID - 10.1016/0021-9290(95)00093-3 [doi]
PST - ppublish
SO  - J Biomech. 1995 Dec;28(12):1451-7. doi: 10.1016/0021-9290(95)00093-3.