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RhoA prevents endotoxin-induced changes in the smooth muscle cell actin cytoskeleton and passive mechanics of pulmonary arteries


, : RhoA prevents endotoxin-induced changes in the smooth muscle cell actin cytoskeleton and passive mechanics of pulmonary arteries. FASEB Journal 16(5): A1120, March 22

Pathological processes can influence the passive arterial mechanics. Therefore, we investigated whether endotoxin exposure alters the passive mechanics of pulmonary arteries, especially in relation to the smooth muscle cell (SMC) F-actin cytoskeleton. We hypothesized that an alteration in the pulmonary passive mechanics might be associated with RhoA, which is known to rearrange the cytoskeleton. We measured passive force-length relations, determined the diameter compliance and visualized the SMC F-actin cytoskeleton by fluorescence staining in the presence or absence of RhoA activation (lysophosphatidic acid; LPA) or Rho kinase inhibition (Y-27632). Endotoxin increased the diameter compliance and induced a chaotic SMC F-actin fiber structure, the latter was in contrast with the regular actin pattern in control arteries. The endotoxin-induced changes of the pulmonary arterial wall properties could be mimicked by cytochalasin B and Rho kinase inhibition and were prevented by co-incubation of the arteries with the RhoA activator LPA. We are the first to show that endotoxin affects the pulmonary SMC passive mechanical properties in relation to the changes in the SMC F-actin cytoskeleton in a RhoA-mediated way. This might be an important aspect of pulmonary artery dysfunction during sepsis and suggests a therapeutic potency for RhoA.

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