gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Effects of hyaluronic acid synthase 2 (HAS2) on the phenotype of human vascular smooth muscle cells

Einfluss der Hyaluronsäuresynthase 2 auf den Phänotyp humaner, glatter Gefäßmuskelzellen

Meeting Abstract (Hypertonie 2004)

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  • M. Sussmann - Institut für Pharmakoloogie und Klinische Pharmakologie (Düsseldorf, D)
  • K. Schrör - Institut für Pharmakoloogie und Klinische Pharmakologie (Düsseldorf, D)
  • J.W. Fischer - Institut für Pharmakoloogie und Klinische Pharmakologie (Düsseldorf, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP18

The electronic version of this article is the complete one and can be found online at:

Published: August 10, 2005

© 2005 Sussmann et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Hyaluronic acid (HA) is a component of the extracellular matrix (ECM) of human atherosclerotic plaques. HA might be involved in the proliferative, migratory and inflammatory response in atherosclerosis. HA synthase 2 (HAS2) is the major HAS2 isoform in smooth muscle cells (SMC) and is induced by a variety of factors that modulate SMC phenotype. In the present study siRNA targeting HAS2 was used to investigate the function of HAS2 in human, vascular SMC. Human VSMC derived from human coronary arteries were used between passages 4-10 and were cultured under standard conditions. HAS2 siRNA and non-silenceing siRNA (control) were transfected using liposome-based transfection procedure. The experiments were initiated 24 hours after transfections. After inducing HAS2 expression by the stable prostacyclin analog iloprost (100 nM) or PDGF-BB inhibition of HAS2 mRNA expression and HA-synthesis by siRNA caused increased spreading of SMC. Subsequently, the phosphorylation of focal adhesion kinase (FAK) at the autophosphorylation site (Y397) was found to be markedly reduced as shown by Western blotting. In addition, the formation of actin stress fibers was enhanced. The levels of cyclin D1, the incorporation of [3H]-thymidine and cell counts were markedly reduced by HAS2-siRNA. The present results suggest that HAS2 interferes with FA-function thereby regulating cell shape and the propensity of SMC to proliferate. These results are in line with a pro-atherosclerotic function of HAS2.