Affiliations: Institute of Biomedical Engineering, West China Center of Medical Sciences, Sichuan University, Chengdu, Sichuan 610041, P.R. China | Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093‐0412, USA | Department Orthopaedics, University of California, San Diego, La Jolla, CA 92093‐0412, USA
Note: [] Address for correspondence: K.‐L. Paul Sung, PhD, Department of Orthopaedics and Bioengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093‐0412, USA. Tel.: +1 858 534 5252; Fax: +1 858 534 6896; E‐mail: klsung@ucsd.edu.
Abstract: We investigated neutrophil activation, specifically F‐actin content and distribution, in situations mimicking the in vivo environment using steady and oscillatory shear. Under low steady shear (<150 s−1) F‐actin levels were decreased for both treated (n‐formyl‐L‐methioryl‐L‐leucyl‐L‐phenylalanine (fMLP)) and untreated neutrophils. The F‐actin content increased with a change to higher steady shear levels. Neutrophils show the same behavior of decreased F‐actin content for oscillatory shear (26.7 s−1) as they did for steady shear. In both situations, the low shear levels caused a decrease in F‐actin content. However, as the magnitude of the shear rate increased, cells showed a reversal to increasing F‐actin content. Shear caused a decrease in F‐actin in the cell cortex for both control and fMLP treated cells. Ctyochalasin B (CB), a common F‐actin assembly blocker, significantly decreased F‐actin content. The results indicate that neutrophils regulate their actin network based on the level and type of shear stress they encounter in the bloodstream.
Keywords: Leukocyte, fluid shear stress, actin
Journal: Biorheology, vol. 41, no. 5, pp. 655-664, 2004
