当前位置： SCI文献检索 > LIFE SCIENCES期刊下所有文献 > Involvement of asymmetric dimethylarginine (ADMA) in glomerular capillary loss and sclerosis in a rat model of chronic kidney disease (CKD).

Involvement of asymmetric dimethylarginine (ADMA) in glomerular capillary loss and sclerosis in a rat model of chronic kidney disease (CKD).

Abstract：

AIMS:Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, has been reported to be a novel marker for the progression of chronic kidney disease (CKD). We have recently found that accumulation of ADMA could trigger peritubular capillary loss, thus contributing to tubulointerstitial ischemia and fibrosis in a rat model of CKD. However, effects of ADMA on glomerular capillary loss and sclerosis remain to be elucidated. MAIN METHODS:In this study, we investigated whether lowering of ADMA by overexpression of dimethylarginine dimethylaminohydrolase (DDAH), a main enzyme that degrades ADMA, could ameliorate glomerular capillary loss and sclerosis in a rat model of CKD. Four weeks after 5/6 subtotal nephrectomy (Nx), animals were given tail vein injections with recombinant adenovirus vector encoding DDAH-I (Adv-DDAH) or control vector expressing bacterial beta-galactosidase (Adv-LZ), or orally administered with 20 mg/kg/day of hydralazine (Hyz) which served as a blood pressure control model. KEY FINDINGS:Plasma levels of ADMA were associated with decreased number of glomerular capillaries as well as severity of glomerular sclerosis in Nx-rats. These glomerular changes progressed in Adv-LZ- or Hyz-treated Nx-rats, while they were ameliorated by the treatment with DDAH overexpression. SIGNIFICANCE:Our present data suggest that ADMA may be involved in glomerular capillary loss and sclerosis, thus contributing to the progression of CKD. Substitution of DDAH protein or enhancement of its activity may become a novel therapeutic strategy for the treatment of CKD.

journal_name

Life Sci

journal_title

Life sciences

authors

Ueda S,Yamagishi S,Matsumoto Y,Kaida Y,Fujimi-Hayashida A,Koike K,Tanaka H,Fukami K,Okuda S

doi

10.1016/j.lfs.2009.03.018

subject

Has Abstract

pub_date

2009-06-05 00:00:00

pages

853-6

issue

23-24

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(09)00143-X

journal_volume

84

pub_type

杂志文章

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