To define the correlation between flow dynamics and the proliferation of arterial smooth muscle cells (SMCs), bovine arterial SMC were subjected to increasing laminar flow shear stress in an in vitro system. Smooth muscle cells were seeded in a fibronectincoated polystyrene cylinder at 5 × 105 cells/tube. The experimental groups were subjected to increasing shear stress (3, 6, 9 dyn cm-2) for a 24-h period. The control group was subjected to similar incubation conditions without flow. Shear stress reduced significantly (p < 0.01) the 24-h incorporation of tritiated thymidine and cell proliferation. This effect was proportional to the level of shear stress and was still evident 24 h after flow cessation. Flow cytometry demonstrated a lower percentage of SMCs in S-phase with increasing shear stress. Extrapolation of these findings to the clinical setting might explain how unphysiological shear stress can predispose to the abnormal proliferation rate of SMCs and early plaque formation. © 1992 Grune & Stratton Ltd.
Modulation of arterial smooth muscle cell growth by haemodynamic forces / Sterpetti, A. V.; Cucina, A.; Santoro, L.; Cardillo, B.; Cavallaro, A.. - In: EUROPEAN JOURNAL OF VASCULAR SURGERY. - ISSN 0950-821X. - 6:1(1992), pp. 16-20. [10.1016/S0950-821X(05)80088-X]
Modulation of arterial smooth muscle cell growth by haemodynamic forces
Sterpetti A. V.
Primo
Membro del Collaboration Group
;Cucina A.;Santoro L.;Cavallaro A.
1992
Abstract
To define the correlation between flow dynamics and the proliferation of arterial smooth muscle cells (SMCs), bovine arterial SMC were subjected to increasing laminar flow shear stress in an in vitro system. Smooth muscle cells were seeded in a fibronectincoated polystyrene cylinder at 5 × 105 cells/tube. The experimental groups were subjected to increasing shear stress (3, 6, 9 dyn cm-2) for a 24-h period. The control group was subjected to similar incubation conditions without flow. Shear stress reduced significantly (p < 0.01) the 24-h incorporation of tritiated thymidine and cell proliferation. This effect was proportional to the level of shear stress and was still evident 24 h after flow cessation. Flow cytometry demonstrated a lower percentage of SMCs in S-phase with increasing shear stress. Extrapolation of these findings to the clinical setting might explain how unphysiological shear stress can predispose to the abnormal proliferation rate of SMCs and early plaque formation. © 1992 Grune & Stratton Ltd.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.