Article

A disintegrin and metalloprotease 17 mediates neointimal hyperplasia in vasculature.

Cardiovascular Research Center, Temple University School of Medicine, 3500 N Broad St, Philadelphia, PA 19140, USA.
Hypertension (impact factor: 6.21). 02/2011; 57(4):841-5. DOI:10.1161/HYPERTENSIONAHA.110.166892 pp.841-5
Source: PubMed

ABSTRACT The requirement of a metalloprotease, a disintegrin and metalloprotease 17 (ADAM17) for the growth of cultured vascular smooth muscle cells has been demonstrated in vitro. However, whether this metalloprotease is responsible for vascular remodeling in vivo remains unanswered. Rat carotid arteries were analyzed 2 weeks after a balloon angioplasty. The neointimal cells were strongly positive for ADAM17 immunostaining. Marked inhibition of intimal hyperplasia was observed in a dominant-negative ADAM17 adenovirus-treated carotid artery. Proliferating cell nuclear antigen-positive cells and phospho-epidermal growth factor receptor-positive cells in the neointima were reduced by dominant-negative ADAM17 as well. In contrast, the neointima formation, proliferating cell nuclear antigen-positive cells, and phospho-epidermal growth factor receptor-positive cells were markedly enhanced by wild-type ADAM17 adenovirus. In conclusion, ADAM17 activation is involved in epidermal growth factor receptor activation and subsequent neointimal hyperplasia after vascular injury. ADAM17 could be a novel therapeutic target for pathophysiological vascular remodeling.

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    Rhian M Touyz
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Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

ADAM17 activation
 
ADAM17 immunostaining
 
balloon angioplasty
 
cultured vascular smooth muscle cells
 
dominant-negative ADAM17
 
dominant-negative ADAM17 adenovirus-treated carotid artery
 
epidermal growth factor receptor activation
 
intimal hyperplasia
 
Marked inhibition
 
metalloprotease 17
 
neointimal cells
 
novel therapeutic target
 
pathophysiological vascular
 
phospho-epidermal growth factor receptor-positive cells
 
Proliferating cell nuclear antigen-positive cells
 
subsequent neointimal hyperplasia
 
unanswered
 
vascular
 
vascular injury
 
wild-type ADAM17 adenovirus