gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Suppression of hyaluronan synthase 3 expression by siRNA inhibits migration and spreading of arterial smooth muscle cells

Unterdrückung der Hyaluronsäuresynthase-3 durch si-RNA, führt zu einer Hemmung der Migration und der Ausbreitung arterieller glatter Muskelzellen

Meeting Abstract

Suche in Medline nach

  • B. Rabausch - Universitätsklinikum Düsseldorf (Düsseldorf, D)
  • M. van den Boom - Universitätsklinikum Düsseldorf (Düsseldorf, D)
  • J.W. Fischer - Universitätsklinikum Düsseldorf (Düsseldorf, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP18

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Veröffentlicht: 8. August 2006

© 2006 Rabausch et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Accumulation of hyaluronic acid (HA) is characteristic for atherosclerotic and restenotic lesions of patients with coronary heart disease. HA, a glycosaminglycan of the extracellular matrix, is synthesized by three HA-synthase (HAS) isoforms, HAS1, HAS2, HAS3. HA regulates a number of fundamental cellular processes such as migration and cell proliferation. However, the functional significance of the individual HAS-isoenzymes is unknown. The aim of the present study was to investigate the function of HAS3 in human arterial smooth muscle cells (SMC). Therefore, specific HAS3-siRNA was used to analyse the effect of HAS3 on migration, proliferation and morphology of SMC. Human arterial SMC were derived from coronary arteries and used between passage 4-10. The cells were cultured in DMEM + 10% FCS ( Fetal Calf Serum) and used at 50-70 % confluency. The cells were transfected with HAS3-siRNA or non-silencing control-siRNA. The experiments were initiated 48h after transfection. HAS3-siRNA reduced HAS3-mRNA levels to 50 ± 22% (n = 4, p<0.05) of control cells. Suppression of HAS3 expression decreased the area occupied by SMC to 59.4 ± 9.2% ( n = 4, p<0.05) of cells treated with control si-RNA. Furthermore, FCS induced migration of SMC was reduced by HAS3-siRNA, as determined by a modified boyden chamber assay (57 ± 8%, n = 3, p< 0.05). Additionally, we examined the effect of HAS3-siRNA on SMC proliferation as assessed by [3H]-thymidine incorporation. HAS3-siRNA transfection inhibited FCS induced DNA synthesis to 63 ± 8% (n = 3, p<0,05) of control cells. These findings demonstrate for the first time that HA synthesized by HAS3 (i) participates in the regulation of cell shape and spreading, (ii) mediates migration and (iii) supports proliferation. These phenotypic characteristics are critical in the development of neointimal hyperplasia and plaque progression. Therefore HAS3 might support the progression of atherosclerosis