Cyclic tensile stretch inhibition of nitric oxide release from osteoblast‐like cells is both G protein and actin‐dependent

Open Access
Publisher Website
Google Scholar
Abstract
Recent reports indicate the alteration of nitric oxide (NO) synthesis with mechanical stress loaded on the osteoblast and NO is considered to have a significant role in mechanotransduction. We found the involvement of guanine‐nucleotide‐binding regulatory proteins (G proteins), especially Gi, in stress‐inhibited NO release of osteoblast‐like cells (JOR:17;593–597, 1999). To determine further the mechanism involved in this process, we measured c‐Jun N‐terminal kinase/stress‐activated protein kinase (JNK/SAPK) activity under cyclic tensile stretch loaded on osteoblast‐like cells. Cyclic stretch significantly enhanced JNK/SAPK activity and pertussis toxin clearly reversed stress‐enhanced JNK/SAPK activity. Cytochalasin D, actin microfilament disrupting reagent, also abolished the stress activation of JNK/SAPK. We propose a model for signaling events induced by cyclic tensile stretch, namely a transmembrane mechanosensor which couples Gi‐protein, actin cytoskeleton and finally activates JNK/SAPK activity of osteoblasts. © 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.

This publication has 29 references indexed in Scilit: