Published January 1, 2010 | Version v1
Journal article

Perfusion of veins at arterial pressure increases the expression of KLF5 and cell cycle genes in smooth muscle cells

  • 1. Section of Molecular Medicine, National Heart and Lung Institute, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ (United Kingdom)
  • 2. Cardiovascular Sciences, Bywaters Center for Vascular Inflammation, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London W12 ONN (United Kingdom)

Description

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 24 h 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.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2009.11.145

Additional details

Identifiers

DOI
10.1016/j.bbrc.2009.11.145;
PII
S0006-291X(09)02341-9;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
391
Journal Issue
1
Journal Page Range
p. 818-823
ISSN
0006-291X
CODEN
BBRCA9

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
45020811
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
BYPASSES; CELL CYCLE; CELL PROLIFERATION; CORONARIES; GENES; GRAFTS; GROWTH FACTORS; MUSCLES; MYOSIN; TISSUE CULTURES; TRANSCRIPTION FACTORS; VEINS
Descriptors DEC
ARTERIES; BLOOD VESSELS; BODY; CARDIOVASCULAR SYSTEM; GLOBULINS; MITOGENS; ORGANIC COMPOUNDS; ORGANS; PROTEINS; TRANSPLANTS

Optional Information

Copyright
Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.