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Proinflammatory Reaction and Cytoskeletal Alterations in Endothelial Cells after Shock Wave Exposure
  1. Anders Sondén,
  2. Anne-Sofie M. Johansson,
  3. Jan Palmblad,
  4. Thomas B. Kjellström
  1. 1From the Department of Surgery (A.S., B.T.K.), Söder Hospital, The Karolinska Institutet, Stockholm, Sweden; Department of Hematology (A.-S.M.J., J.P.), Karolinska University Hospital Huddinge, Stockholm, Sweden; and Defense Medicine (B.T.K.), Swedish Defense Research Agency, Stockholm, Sweden.
  1. Funding was provided by the Swedish Defense Research Agency, Stockholm, Sweden (Grant # E 5055), The Swedish Medical Research Council (Grant 19 x-5991), and The Fund of King Gustav V.
  2. Address correspondence to: Dr. Anders Sondén, Department of Surgery, Söder Hospital, SE-118 83 Stockholm, Sweden; tel: +46-8-6161000; fax: +46-8-6161360; e-mail: anders.sonden{at}sos.ki.se

Abstract

Background Although the effects on human organs by shock waves (SWs) induced by medical treatments or high-energy trauma are well recognized, little is known about the effects on the cellular level. Since blood vessel injury is a common finding after SW exposure, we assessed the in vitro effects of SWs on human umbilical vein endothelial cells (HUVECs).

Methods An in vitro trauma model was used to expose HUVEC monolayers to focused SWs or to shock waves plus cavitation (SWC), a subsequent phenomenon that is often considered the main cause of SW vascular injury.

Results SWs alone did not cause any changes in the studied variables. In contrast, HUVEC monolayers exposed to SWC exhibited discrete central lesions with extensive cell death. Cells peripheral to the main lesion area displayed disassembly of dense peripheral bands and formation of actin stress fibers, indicating increased intercellular gaps. Expression of P-selectin was enhanced 11-fold compared with controls, whereas expression of E-selectin and intercellular adhesion molecule 1 was enhanced 8-fold (p < .05) and 1.5-fold (p < .01), respectively. The latter responses were preceded by nuclear translocation of nuclear factor κB subunit p65 by 16% (p < .01). When compared with mechanically produced lesions used as controls, SWC lesions exhibited an impaired regeneration rate of the endothelial cell layer (p < .001). Redistribution of centrosomes toward the lesion borders was less effective in the SWC samples compared with the mechanically produced lesions (p < .01).

Conclusions SWC lesions were associated with a switch to an endothelial proinflammatory phenotype, with an impaired regeneration rate and changes in cytoskeletal functions.

Key Words
  • shock waves
  • endothelium
  • inflammation

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