Article

Low molecular weight fucoidan prevents intimal hyperplasia in rat injured thoracic aorta through the modulation of matrix metalloproteinase-2 expression.

INSERM U698, Bio-ingénierie Cardiovasculaire, Université Paris 13, France.
Biochemical pharmacology (impact factor: 4.25). 09/2010; 81(2):233-43. DOI:10.1016/j.bcp.2010.09.021 pp.233-43
Source: PubMed

ABSTRACT The therapeutic potential of low molecular-weight fucoidan (LMWF), a sulfated polysaccharide extracted from brown seaweed was investigated on vascular smooth muscle cell (VSMC) and human vascular endothelial cell (HUV-EC-C) proliferation and migration in vitro and in a rat model of intimal hyperplasia. Sprague-Dawley rats were subjected to balloon injury in the thoracic aorta followed by two weeks' treatment with either LMWF (5mg/kg/day) or vehicle. Morphological analysis and proliferating cell nuclear antigen immunostaining at day 14 indicated that LMWF prevented intimal hyperplasia in rat thoracic aorta as compared with vehicle (neo-intima area, 3±0.50mm(2) versus 5±0.30mm(2), P<0.01). In situ zymography showed that LMWF significantly decreased the activity of matrix metalloproteinase (MMP)-2 in the neo-intima compared to vehicle. The in vitro study demonstrated that 10μg/ml LMWF increased HUV-EC-C migration by 45±5% but reduced VSMC migration by 40±3%. LMWF also increased MMP-2 mRNA expression in HUV-EC-Cs and reduced it in VSMCs. MMP-2 level in the conditioned medium from cells incubated with 10μg/ml LMWF was 5.4-fold higher in HUV-EC-Cs, but 6-fold lower in VSMCs than in untreated control cells. Furthermore, decreasing MMP-2 expression in HUV-EC-Cs or VSMCs by RNA interference resulted in reduced LMWF-induced effects on cell migration. In conclusion, LMWF increased HUV-EC-C migration and decreased VSMC migration in vitro. In vivo, this natural compound reduced the intimal hyperplasia in the rat aortic wall after balloon injury. Therefore, LMWF could be of interest for the prevention of intimal hyperplasia.

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Keywords

6-fold lower
 
balloon injury
 
brown seaweed
 
cell migration
 
cells incubated
 
conditioned medium
 
decreasing MMP-2 expression
 
human vascular endothelial cell
 
HUV-EC-C migration
 
intimal hyperplasia
 
MMP-2 level
 
MMP-2 mRNA expression
 
proliferating cell nuclear antigen immunostaining
 
rat thoracic aorta
 
RNA interference
 
Sprague-Dawley rats
 
sulfated polysaccharide
 
untreated control cells
 
vascular smooth muscle cell
 
VSMC migration