Mechanical strain induces a persistent upregulation of syndecan-1 expression in smooth muscle cells

✍ Scribed by Matheau A. Julien; Carolyn A. Haller; Peiyi Wang; Jing Wen; Elliot L. Chaikof

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 181 KB
• Volume: 211
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.20927

✦ Synopsis

Abstract

Syndecan‐1 belongs to a family of transmembrane proteoglycans, acts as a coreceptor for growth factor binding, as well as cell–matrix and cell–cell interactions, and is induced in smooth muscle cells (SMCs) following balloon catheter injury. In this report, we investigated syndecan‐1 expression in SMCs in response to several distinct biomechanical force profiles and the related syndecan shedding response. Syndecan‐1 mRNA expression increased in response to 5% and 10% cyclic strain (24 h: 206 ± 40% and 278 ± 33%, respectively, P < 0.05) when compared to unstrained controls. When subjected to 10% cyclic strain for periods of up to 48 h, syndecan‐1 mRNA levels remained elevated at 294 ± 31%. Notably, the SMC mechanosensor mechanism remained responsive after an initial 24 h “preconditioning” period, as evident by a fivefold increase in syndecan‐1 gene expression following a change in cyclic stress from 10% to 20% (48 h: 516 ± 55%, P < 0.05). Of note, similar behavior was not observed in an analysis of syndecan‐2 mRNA levels. Commensurate with mRNA responses, mechanical stress induced an increase in cell‐associated syndecan‐1 protein levels with an associated increase in protein shedding. Given the varied functions of syndecan‐1, stress‐induced effects on SMC syndecan‐1 expression and shedding may represent an additional component of the pro‐inflammatory, growth‐stimulating pathways that are activated in response to changes in the mechanical microenvironment of the vascular wall. Syndecan‐1 expression is uniquely influenced by changes in the phase and magnitude of the local stress field. J. Cell. Physiol. 211: 167–173, 2007. © 2006 Wiley‐Liss, Inc.