PMID- 12817708
OWN - NLM
STAT- MEDLINE
DCOM- 20030721
LR  - 20190402
IS  - 0304-4920 (Print)
IS  - 0304-4920 (Linking)
VI  - 45
IP  - 4
DP  - 2002 Dec 31
TI  - Shear stress attenuates tumor necrosis factor-alpha-induced monocyte chemotactic 
      protein-1 expressions in endothelial cells.
PG  - 169-76
AB  - The interplay between shear stress and cytokines in regulating vascular 
      endothelial function remains largely unexplored. In the present study, the 
      potential role of shear stress in regulating tumor necrosis factor-alpha 
      (TNF-alpha)-induced gene expression in endothelial cells (ECs) was investigated. 
      The TNF-alpha-induced monocyte chemotactic protein-1 (MCP-1) mRNA expressions 
      were significantly attenuated in ECs subjected to a high level of shear stress 
      (20 dynes/cm2) for 4 or 24 h prior to the addition of TNF-alpha in the presence 
      of flow. Less inhibition of TNF-alpha-induced MCP-1 mRNA expression was found in 
      ECs pre-exposed to a low level of shear stress (1.2 dynes/cm2) for 24 h as 
      compared with the cells presheared (pre-exposed to shear stress) for 4 h. 
      Simultaneous exposure of ECs to TNF-alpha and a high or low level of shear stress 
      down-regulated TNF-alpha-induced MCP-1 gene expressions, suggesting that the 
      post-flow condition modulates endothelial responses to cytokine stimulation. 
      Individually or combined, an endothelial nitric oxide synthase (eNOS) inhibitor 
      and a glutathione (GSH) biosynthesis inhibitor had no effect on this shear 
      stress-mediated inhibition. Moreover, in ECs either presheared or remained in a 
      static condition prior to stimulation by TNF-alpha while under shear flow, the 
      ability of TNF-alpha to induce AP-1-DNA binding activity in the nucleus was 
      reduced. Our findings suggest that shear stress plays a protective role in 
      vascular homeostasis by inhibiting endothelial responses to cytokine stimulation.
FAU - Chiu, Jeng-Jiann
AU  - Chiu JJ
AD  - Division of Medical Engineering Research, National Health Research Institutes, 
      Taipei 114, Taiwan, ROC. jjchiu@nhri.org.tw
FAU - Lee, Pei-Ling
AU  - Lee PL
FAU - Lee, Chih-I
AU  - Lee CI
FAU - Chen, Li-Jing
AU  - Chen LJ
FAU - Chen, Cheng-Nan
AU  - Chen CN
FAU - Ko, Ya-Chen
AU  - Ko YC
FAU - Lien, Sheng-Chieh
AU  - Lien SC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - India
TA  - Chin J Physiol
JT  - The Chinese journal of physiology
JID - 7804502
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 27JT06E6GR (omega-N-Methylarginine)
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
EIN - Chin J Physiol. 2003 Mar 31;46(1):39
MH  - Antineoplastic Agents/*pharmacology
MH  - Cell Nucleus/metabolism
MH  - Chemokine CCL2/*genetics
MH  - Endothelium, Vascular/cytology/*physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Expression/drug effects/physiology
MH  - Glutathione/metabolism
MH  - Humans
MH  - Monocytes/physiology
MH  - Nitric Oxide Synthase/antagonists & inhibitors/metabolism
MH  - Nitric Oxide Synthase Type III
MH  - Oxidation-Reduction
MH  - Stress, Mechanical
MH  - Transcription Factor AP-1/metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Umbilical Cord/cytology
MH  - omega-N-Methylarginine/pharmacology
EDAT- 2003/06/24 05:00
MHDA- 2003/07/23 05:00
CRDT- 2003/06/24 05:00
PHST- 2003/06/24 05:00 [pubmed]
PHST- 2003/07/23 05:00 [medline]
PHST- 2003/06/24 05:00 [entrez]
PST - ppublish
SO  - Chin J Physiol. 2002 Dec 31;45(4):169-76.