Low molecular weight fucoidan prevents neointimal hyperplasia after
aortic allografting.
* Freguin-Bouilland C
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Freguin%2DBouilland+C%22%5BAuthor%5D> ,
* Alkhatib B
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Alkhatib+B%22%5BAuthor%5D> , * David N
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22David+N%22%5BAuthor%5D> , * Lallemand
F
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Lallemand+F%22%5BAuthor%5D> , * Henry
JP
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Henry+JP%22%5BAuthor%5D> , * Godin M
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Godin+M%22%5BAuthor%5D> , * Thuillez C
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Thuillez+C%22%5BAuthor%5D> , *
Plissonnier D
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itoo\
l=pubmed_AbstractPlus&term=%22Plissonnier+D%22%5BAuthor%5D> .

1 Inserm U644, IFRMP 23, Rouen University Hospital-Charles Nicolle,
Rouen, France. 2 Nephrology Department, Rouen University Hospital, Bois
Guillaume, France.

BACKGROUND.: Fucoidan, a new low molecular weight sulfated
polysaccharide (LMWF), has previously been shown to mobilize bone
marrow-derived progenitors cells via stimulation of stromal derived
factor (SDF)-1 release. Mobilized progenitor cells have been suggested
to repair intimal lesions after immune-mediated endothelial injury and
thus prevent intimal proliferation. The aim of this study was to
evaluate the effect of LMWF treatment in a rat aortic allograft model of
transplant arteriosclerosis (TA). METHODS.: Aortic grafts were performed
in Brown Norway (BN, donor) and Lewis (Lew, recipient) rats. The
recipient rats were treated with LMWF (5 mg/kg/day) and sacrificed at 30
days. To determine the role of SDF-1 in mediating the effects of LMWF, a
specific inhibitor of the SDF-1 receptor CXCR4, AMD 3100 (20
mug/kg/day), was used. The grafted segments were evaluated by
morphometric (histochemical) analyses. RESULTS.: Untreated aortic
allografts exhibited severe intimal proliferation, indicative of TA. In
contrast, LMWF treatment significantly prevented allograft intimal
proliferation as compared with controls (5.7+/-3 vs. 66.2+/-6 mum,
P<0.01) and permitted a normalization of the intima/media ratio
(0.1+/-0.1 vs. 1.7+/-0.3, P<0.01). Further, LMWF treatment stimulated
allograft reendothelialization, as evidenced by strong intimal
endothelial nitric oxide synthase antibody and CD31 signals.
Unexpectedly, AMD treatment failed to prevent the protective effect of
LMWF on intimal thickening and AMD treatment alone was found to reduced
intimal proliferation in allografts. CONCLUSIONS.: We found that LMWF
treatment reduced intimal thickness and induced the presence of an
endothelial cell lining in the vascular graft at 30 days. Our findings
may suggest a novel therapeutic strategy in the prevention of TA.

PMID: 17496541 [PubMed - in process]



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