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.2009.11.145Additional 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.