کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2070311 | 1544495 | 2008 | 21 صفحه PDF | دانلود رایگان |
We studied which components of mechanical cell deformation are involved in “stretch modulated ion currents” (SMIC). Murine ventricular myocytes were attached to glass coverslips and deformed in x, y and z with a 16 μm thin glass stylus (S) of calibrated stiffness. Three-dimensional confocal microscopy characterized cell deformation (T-tubular membranes, mitochondria) and bending of S (indicative of the applied force). Axial (x-) displacement of S sheared the upper cell part versus the attached bottom, close to S, it changed sarcomere length and bent z-lines (“z-line displacement”). Vertical (z-press) or transversal (y-shear) displacement of S bulged cytoplasm and mitochondria transversally without detectable z-line displacement.Axial stiffness increased with the extent of stress (“stress stiffening”). Depolymerization of F-actin or block of integrin receptors reduced stiffness. SMIC served as a proxy readout of deformation-induced signaling. Axial deformation activated a non-selective cation conductance (Gns) and deactivated an inwardly rectifying K+ conductance (GK1), z-press or y-shear did not induce SMIC. Depolymerization of F-actin or block of integrin receptors reduced SMIC. SMIC did not depend on changes in sarcomere length but correlated with the extent of z-line bending. We discuss that both shear stress at the attached cell bottom and z-line bending could activate mechanosensors. Since SMIC was absent during deformations without z-line bending we postulate that z-line bending is a necessary component for SMIC signaling.
Journal: Progress in Biophysics and Molecular Biology - Volume 97, Issues 2–3, June–July 2008, Pages 196–216