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Rivista di Angiologia
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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International Angiology 2000 March;19(1):39-46
Direct and indirect effects of pulsatile shear stress on the smooth muscle cell
Shigematsu K., Yasuhara H., Shigematsu H., Muto T.
From the Division of Vascular Surgery, Department of Surgery, The University of Tokyo, Tokyo, Japan
Background. Anastomotic intimal hyperplasia is still an unsolved problem after small caliber prosthetic bypass grafting. Oscillatory turbulent flow occurs at the end to side anastomosis, and produces various effects on smooth muscle cells (SMCs) and endothelial cells (ECs), which compose intimal hyperplasia. We examined the influences of pulsatile oscillating shear stress on SMCs mitogenic activity induced by sheared ECs.
Methods. 1) SMCs were cultured under three different pulsatile shear conditions (mean: 0, 6, and 60 dyne/cm2).
2) ECs were cultured under both static and sheared condition (mean: 60 dyne/cm2). Using the conditioned media from each well, SMCs were cultured under static and sheared conditions (60 dyne/cm2). Four groups of SMCs were devised by combining the two types of media and the two culture conditions. SMC colony spreading distances were measured as an index of combined migration and proliferation activity. An MTT assay and a cell counting assay were used to determine the proliferation activities of SMCs.
Results. 1) SMC spreading activity was suppressed by shear stress. SMC proliferative activity was stimulated by pulsatile turbulent shear stress. 2) SMC spreading activity was stimulated by mitogens derived from ECs under shear stress. However, this augmented SMC spreading activity was attenuated under sheared conditions. The mitogens derived from ECs under pulsatile shear stress had no effects on SMC proliferation activity.
Conclusions. Pulsatile oscillating shear stress attenuates SMC migration activity induced by EC-derived mitogens and stimulates SMC proliferative activity.