help button home button Biophys. J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pritchard, S.
Right arrow Articles by Guilak, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pritchard, S.
Right arrow Articles by Guilak, F.

Biophys J, November 2002, p. 2502-2510, Vol. 83, No. 5

Hyperosmotically Induced Volume Change and Calcium Signaling in Intervertebral Disk Cells: The Role of the Actin Cytoskeleton

Scott Pritchard,*dagger Geoffrey R. Erickson,*dagger and Farshid Guilak*dagger Dagger

Departments of  *Surgery,  dagger Biomedical Engineering, and  Dagger Mechanical Engineering and Materials Science, Duke University Medical Center, Durham, North Carolina 27710 USA

Loading of the spine alters the osmotic environment in the intervertebral disk (IVD) as interstitial water is expressed from the tissue. Cells from the three zones of the IVD, the anulus fibrosus (AF), transition zone (TZ), and nucleus pulposus (NP), respond to osmotic stress with altered biosynthesis through a pathway that may involve calcium (Ca2+) as a second messenger. We examined the hypothesis that IVD cells respond to hyperosmotic stress by increasing the concentration of intracellular calcium ([Ca2+]i) through a mechanism involving F-actin. In response to hyperosmotic stress, control cells from all zones decreased in volume and cells from the AF and TZ exhibited [Ca2+]i transients, while cells from the NP did not. Extracellular Ca2+ was necessary to initiate [Ca2+]i transients. Stabilization of F-actin with phalloidin prevented the Ca2+ response in AF and TZ cells and decreased the rate of volume change in cells from all zones, coupled with an increase in the elastic moduli and apparent viscosity. Conversely, actin breakdown with cytochalasin D facilitated Ca2+ signaling while decreasing the elastic moduli and apparent viscosity for NP cells. These results suggest that hyperosmotic stress induces volume change in IVD cells and may initiate [Ca2+]i transients through an actin-dependent mechanism.

Biophys J, November 2002, p. 2502-2510, Vol. 83, No. 5
© 2002 by the Biophysical Society   0006-3495/02/11/2502/09  $2.00


This article has been cited by other articles:


Home page
 JBJSHome page
L. A. Setton and J. Chen
Mechanobiology of the Intervertebral Disc and Relevance to Disc Degeneration
J. Bone Joint Surg. Am., April 1, 2006; 88(suppl_2): 52 - 57.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 by the Biophysical Society.