Perfusion of veins at arterial pressure increases the expression of KLF5 and cell cycle genes in smooth muscle cells.
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.
Amirak
Emre
E
Section of Molecular Medicine, National Heart and Lung Institute, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ, UK.
Zakkar
Mustafa
M
Evans
Paul C
PC
Kemp
Paul R
PR
D000818:Animals; D001794:Blood Pressure / Q000235:genetics*; D002453:Cell Cycle / Q000235:genetics*; D049109:Cell Proliferation; D056741:Cyclin D / Q000235:genetics; D019927:Cyclin E / Q000235:genetics; D005786:Gene Expression Regulation; D051741:Kruppel-Like Transcription Factors / Q000235:genetics*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics; D013552:Swine; D014680:Veins / Q000166:cytology / Q000378:metabolism*
D056741:Cyclin D; D019927:Cyclin E; D051741:Kruppel-Like Transcription Factors; D016271:Proto-Oncogene Proteins c-myc