Exp Clin Endocrinol Diabetes 2004; 112(7): 356-363
DOI: 10.1055/s-2004-821014
Article

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Fluid Shear of Low Magnitude Increases Growth and Expression of TGFβ1 and Adhesion Molecules in Human Bone Cells in Vitro

U. M. Liegibel1 , U. Sommer1 , B. Bundschuh1 , B. Schweizer2 , U. Hilscher1 , A. Lieder1 , P. Nawroth1 , C. Kasperk1
  • 1Endocrinology and Metabolism, Department of Medicine, Ruprecht-Karls-University, Heidelberg, Germany
  • 2Institute of Applied Mathematics, Ruprecht-Karls-University, Heidelberg, Germany
Further Information

Publication History

Received: July 31, 2003 First decision: October 15, 2003

Accepted: February 26, 2004

Publication Date:
07 July 2004 (online)

Abstract

Deformation of the bone matrix by mechanical strain causes fluid shifts within the osteocytic canaliculi which affect osteocytic cell metabolism. We applied low fluid shear (1 - 63 µPa for 10 - 48 h) to human osteoblastic cells (HOB) in vitro to study its impact on cell proliferation and differentiated functions. Proteins involved in translating the physical force into a cellular response were characterised. Low fluid shear stress stimulated proliferation of HOB 1.2-fold when stress was applied intermittently for 24 h. Shear stress also increased differentiated cellular properties such as alkaline phosphatase (ALP) activity (121 % of control), fibronectin (FN) and fibronectin receptor (FNR) expression (290 % and 200 %, respectively). Prostaglandin E2 (PGE2) and TGFβ1 release into the medium were significantly stimulated when shear stress was applied for 6 - 12 h and 24 - 48 h, respectively. TGFβ1 + 2 neutralising antibodies or the presence of indomethacine inhibited the mitogenic effect of fluid shear and reduced ALP activity to its control level. Furthermore, TGFβ treatment induced a dose-dependent increase in FN and FNR expression. Therefore, fluid shear stress of low magnitude (a) suffices to affect HOB metabolism and (b) regulates anchorage of HOB via FN and FNR by stimulating osteoblastic PGE2 and TGFβ secretion.

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Dr. Christian Kasperk

Ruprecht-Karls-University
Department of Medicine I/Endocrinology and Metabolism

Luisenstraße 5

69115 Heidelberg

Germany

Phone: + 496221568604

Fax: + 49 62 21 56 43 59

Email: Christian.Kasperk@med.uni-heidelberg.de