Protection of DDAH2 Overexpression Against Homocysteine-Induced Impairments of DDAH/ADMA/NOS/NO Pathway in Endothelial Cells | Zendy

Lihua Liu | Zendy; Zheng Guo | Zendy; Mei Feng | Zendy; Zhong-Zu Wu | Zendy; Zhimin He | Zendy; Yan Xiong | Zendy

Open Access

Protection of DDAH2 Overexpression Against Homocysteine-Induced Impairments of DDAH/ADMA/NOS/NO Pathway in Endothelial Cells

Author(s) -

Lihua Liu,

Zheng Guo,

Mei Feng,

Zhong-Zu Wu,

Zhimin He,

Yan Xiong

Publication year - 2012

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000343329

Subject(s) - asymmetric dimethylarginine , endothelial dysfunction , hyperhomocysteinemia , homocysteine , medicine , endothelial stem cell , enos , endogeny , endothelium , nitric oxide , endocrinology , nitric oxide synthase , endothelial nos , chemistry , arginine , biochemistry , in vitro , amino acid

Homocysteine-induced endothelial dysfunction favors the development of cardiovascular diseases through accumulation of endogenous nitric oxide (NO) synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA). Dimethylarginine dimethylaminohydrolase 2 (DDAH2) is the major enzyme for the degradation of ADMA in endothelial cells. The purpose of this study was to determine whether suppressed DDAH2 expression contributed to impairments of DDAH/ADMA/NOS/NO pathway induced by homocysteine in endothelial cells and whether DDAH2 overexpression could prevent endothelial cell dysfunction caused by homocysteine.

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