HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 555/2/565    most recent jphysiol.2003.059899v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by White, C. R. Articles by Frangos, J. A. Search for Related Content PubMed PubMed Citation Articles by White, C. R. Articles by Frangos, J. A.

Charles R. White^,1,2, Mark A. Haidekker^,3, Hazel Y. Stevens¹ and John A. Frangos¹

¹ La Jolla Bioengineering Institute, 505 Coast Boulevard South, La Jolla, CA 92037, USA² Loma Linda University, Center for Perinatal Biology, Loma Linda, CA 92350, USA³ University of Missouri–Columbia, Department of Biological Engineering, Columbia, MO 65211-2200, USA

Hand–arm vibration syndrome is a vascular disease of occupational origin and a form of secondary Raynaud's phenomenon. Chronic exposure to hand-held vibrating tools may cause endothelial injury. This study investigates the biomechanical forces involved in the transduction of fluid vibration in the endothelium. Human endothelial cells were exposed to direct vibration and rapid low-volume fluid oscillation. Rapid low-volume fluid oscillation was used to simulate the effects of vibration by generating defined temporal gradients in fluid shear stress across an endothelial monolayer. Extracellular signal-regulated kinase (ERK1/2) phosphorylation and endothelin-1 (ET-1) release were monitored as specific biochemical markers for temporal gradients and endothelial response, respectively. Both vibrational methods were found to phosphorylate ERK1/2 in a similar pattern. At a fixed frequency of fluid oscillation where the duration of each pulse cycle remained constant, ERK1/2 phosphorylation increased with the increasing magnitude of the applied temporal gradient. However, when the frequency of flow oscillation was increased (thus decreasing the duration of each pulse cycle), ERK1/2 phosphorylation was attenuated across all temporal gradient flow profiles. Fluid oscillation significantly stimulated ET-1 release compared to steady flow, and endothelin-1 was also attenuated with the increase in oscillation frequency. Taken together, these results show that both the absolute magnitude of the temporal gradient and the frequency/duration of each pulse cycle play a role in the biomechanical transduction of fluid vibrational forces in endothelial cells. Furthermore, this study reports for the first time a link between the ERK1/2 signal transduction pathway and transmission of vibrational forces in the endothelium.

(Received 16 December 2003; accepted after revision 23 December 2003; first published online 9 January 2004)
Corresponding author J. A. Frangos: La Jolla Bioengineering Institute, 505 Coast Boulevard South, La Jolla, CA 92037, USA.  Email: frangos{at}ljbi.org

This article has been cited by other articles:

				V. K. Sidhaye, K. S. Schweitzer, M. J. Caterina, L. Shimoda, and L. S. King Shear stress regulates aquaporin-5 and airway epithelial barrier function PNAS, March 4, 2008; 105(9): 3345 - 3350. [Abstract] [Full Text] [PDF]

				A. Thompson and R. House Hand-arm vibration syndrome with concomitant arterial thrombosis in the hands Occup. Med., August 1, 2006; 56(5): 317 - 321. [Abstract] [Full Text] [PDF]

				P. B. Furspan, S. Chatterjee, M. D. Mayes, and R. R. Freedman Cooling-induced contraction and protein tyrosine kinase activity of isolated arterioles in secondary Raynaud's phenomenon Rheumatology, April 1, 2005; 44(4): 488 - 494. [Abstract] [Full Text] [PDF]