Document Detail


Perfusion of veins at arterial pressure increases the expression of KLF5 and cell cycle genes in smooth muscle cells.
MedLine Citation:
PMID:  19958749     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vascular smooth muscle cell (VSMC) proliferation remains a major cause of veno-arterial graft failure. We hypothesised that exposure of venous SMCs to arterial pressure would increase KLF5 expression and that of cell cycle genes. Porcine jugular veins were perfused at arterial or venous pressure in the absence of growth factors. The KLF5, c-myc, cyclin-D and cyclin-E expression were elevated within 24h of perfusion at arterial pressure but not at venous pressure. Arterial pressure also reduced the decline in SM-myosin heavy chain expression. These data suggest a role for KLF5 in initiating venous SMCs proliferation in response to arterial pressure.
Authors:
Emre Amirak; Mustafa Zakkar; Paul C Evans; Paul R Kemp
Related Documents :
8024449 - A comparison of the cuff deflation method with valsalva's maneuver and limb compression...
6869029 - Effect of chronic sympathetic denervation upon the transcapillary filtration rate induc...
19029009 - Inelastic compression increases venous ejection fraction more than elastic bandages in ...
8086729 - Accuracy of central venous pressure measurements in the inferior vena cava in the venti...
7249009 - Femoral vein pressure measurements for evaluation of venous function in patients with p...
6703289 - Venous pressure and arm volume changes during simulated bier's block.
14763049 - Complications of peritoneal dialysis related to increased intra-abdominal pressure.
10611919 - An adult case with an abnormal right ventricular structure causing intraventricular pre...
2129469 - Antiproteinuric effect of angiotensin-converting-enzyme inhibitors in patients with pri...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-02
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  391     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-27     Completed Date:  2010-03-15     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  818-23     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / genetics*
Cell Cycle / genetics*
Cell Proliferation*
Cyclin D / genetics
Cyclin E / genetics
Gene Expression Regulation*
Kruppel-Like Transcription Factors / genetics*
Myocytes, Smooth Muscle / metabolism*
Proto-Oncogene Proteins c-myc / genetics
Swine
Veins / cytology,  metabolism*
Grant Support
ID/Acronym/Agency:
FS/10/006/27960//British Heart Foundation; PG/09/088/28058//British Heart Foundation; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Cyclin D; 0/Cyclin E; 0/Kruppel-Like Transcription Factors; 0/Proto-Oncogene Proteins c-myc
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The stimulatory effect of angiotensin II on Na(+)-ATPase activity involves sequential activation of ...
Next Document:  Efficient inhibition of the formation of joint adhesions by ERK2 small interfering RNAs.