Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury.

Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Research Abstract Details 

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Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Abstract Text:

Hakuoh Konishi,Karsten Sydow,John P Cooke,

OBJECTIVES: We sought to determine if a reduction in asymmetric dimethylarginine (ADMA) enhances endothelial regeneration. BACKGROUND: Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthase (NOS). Increased plasma levels of ADMA are associated with endothelial vasodilator dysfunction in patients with vascular disease or risk factors. Asymmetric dimethylarginine is eliminated largely by the action of dimethylarginine dimethylaminohydrolase (DDAH), which exists in 2 isoforms. Dimethylarginine dimethylaminohydrolase-1 transgenic (TG) mice manifest increased DDAH activity, reduced plasma and tissue ADMA levels, increased nitric oxide synthesis, and reduced systemic vascular resistance. METHODS: The left femoral arteries of DDAH1 TG mice and wild-type (WT) mice were injured by a straight spring wire, and regeneration of the endothelial cell (EC) monolayer was assessed. Endothelial sprouting was assayed with growth factor-reduced Matrigel. RESULTS: Regeneration of the EC monolayer was more complete 1 week after injury in TG mice (WT vs. TG: 40.0 +/- 6.5% vs. 61.2 +/- 6.4%, p < 0.05). The number of CD45 positive cells at the injured sites was reduced by 62% in DDAH TG mice (p < 0.05). Four weeks after injury, the neointima area and intima/media ratio were attenuated in DDAH TG mice (WT vs. TG: 0.049 +/- 0.050 mm2 vs. 0.031 +/- 0.060 mm2, 3.1 +/- 0.5 vs. 1.7 +/- 0.2, respectively, p < 0.05). Endothelial cell sprouting from vascular segments increased in TG mice (WT vs. TG: 24.3 +/- 3.9 vs. 39.0 +/- 2.2, p < 0.05). CONCLUSIONS: We find for the first time an important role for DDAH in EC regeneration and in neointima formation. Strategies to enhance DDAH expression or activity might be useful in restoring the endothelial monolayer and in treating vascular disease.

Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Publishing Authors By Initials

H Konishi,K Sydow,JP Cooke,

For similar cardiovascular diseases: vascular diseases research abstracts see: cardiovascular diseases: vascular diseases research

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Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of the American College of Cardiology

VOLUME: 49

Page Numbers: 1099-105

Journal Abbreviation: J. Am. Coll. Cardiol.

ISSN: 1558-3597

DAY: 23

MONTH: 02

YEAR: 2007

Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8301365

Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Keywords Mesh Terms:

KEYWORDS: Vascular Diseases

MESH TERMS: pathology

Chemical & Substance for Abstract: Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury. Information

Substance Name: dimethylargininase

Registry Number: EC 3.5.3.18

Grant and Affiliation Information for Dimethylarginine dimethylaminohydrolase promotes endothelial repair after vascular injury.

AFFILIATION: Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL63685

ACRONYM: HL

MEDLINETA: J Am Coll Cardiol

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