Reference : Co-cultures of Human Coronary Smooth Muscle Cells and Dimethyl Sulfoxide-differentiat... |
Scientific journals : Article | |||
Life sciences : Biochemistry, biophysics & molecular biology | |||
http://hdl.handle.net/10993/5692 | |||
Co-cultures of Human Coronary Smooth Muscle Cells and Dimethyl Sulfoxide-differentiated HL60 Cells Upregulate ProMMP9 Activity and Promote Mobility"”Modulation By Reactive Oxygen Species | |
English | |
Bernard, Yohann [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >] | |
Melchior, Chantal [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >] | |
Tschirhart, Eric ![]() | |
Bueb, Jean-Luc ![]() | |
2008 | |
Inflammation | |
Springer Netherlands | |
1-2 | |
Yes (verified by ORBilu) | |
0360-3997 | |
[en] atherosclerosis ; inflammation ; oxidative stress ; matrix metalloproteinases ; cell migration | |
[en] Vascular cells and leukocytes, involved in the development of atherosclerosis, produce cytokines and/or reactive oxygen species (ROS) and matrix metalloproteinases (MMPs) implicated in cell mobility. We investigated by co-culture experiments the effects of human coronary smooth muscle cells (HCSMC) on MMPs characteristics and mobility of neutrophil-like dimethyl sulfoxide-differentiated HL60 cells (≠HL60). The effects of superoxide dismutase (SOD) and catalase were also analyzed. All the studied MMP2 characteristics remained unchanged. HCSMC stimulated MMP9 protein level, activity and mobility of ≠HL60 cells and expressed and secreted a variety of cytokines implicated in atherosclerosis. SOD and catalase increased MMP9 expression, protein level and activity of ≠HL60, but migration of ≠HL60 cells was only decreased by catalase, demonstrating that ROS are more efficient in modulating MMP9 activity of ≠HL60 than their mobility. Finally, HCSMC being able to stimulate ≠HL60, their co-cultures may represent an in vitro approach to study cellular interactions occurring in vivo during atherosclerosis. | |
http://hdl.handle.net/10993/5692 | |
10.1007/s10753-008-9077-z |
There is no file associated with this reference.
All documents in ORBilu are protected by a user license.