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Results 1 - 7 of 7
EC Number
General Information
Commentary
Reference
malfunction
DDAH1 knockout impairs endothelial sprouting from cultured aortic rings, and overexpression of constitutively active Akt or DDAH1 rescues endothelial sprouting in the aortic rings from these mice
malfunction
plasma and tissue asymmetrical dimethylarginine (ADMA) and N-monomethyl-L-arginine (L-NMMA) levels in DDAH1-/- mice are several folds higher than in wild-type mice, but growth and development of these knockout mice are similar to wild-type. Although the expression of DDAH2 is unaffected, DDAH activity is undetectable in all tissues tested. Results indicate that DDAH1 is the critical enzyme for ADMA and L-NMMA degradation
malfunction
using selective gene silencing of DDAH1 with small interfering RNA and overexpression of DDAH1 in HUVEC, it is shown that DDAH1 acts to promote endothelial cell proliferation, migration and tube formation both by Akt phosphorylation as well as through the traditional role of degrading ADMA. DDAH1 overexpression increases Ras activity
physiological function
heterozygous DDAH1 embryos express DDAH1 RNA and protein at approximately 50% of wild-type levels, while circulating plasma asymmetric dimethylarginine levels of heterozygotes are about 20% higher than those of wild-type mice. Homozygous DDAH1 null embryos are generated at low frequency, and do not progress through embryonic development. Mice carrying an inactivated DDAH2 locus have reduced DDAH2 expression at both the RNA and protein levels in all tissues studied. Breeding of these mice indicates that both heterozygous and homozygous inactivation of the DDAH2 locus does not impact on embryonic survival, with wild type, heterozygous and null mice produced in Mendelian ratios
physiological function
human DDAH1 overexpression does not protect against hypertension-induced cardiac fibrosis and hypertrophy. In addition, the hypertension-induced impairment of the endothelium-dependent vasorelaxation of aortic segments ex vivo is not significantly attenuated by DDAH1 overexpression. However, human DDAH1 overexpressing mice display an attenuated hypertensive inflammatory response in renal tissue, resulting in less hypertensive renal injury
physiological function
overexpression of DDAH-1 increases endothelial nitric oxide by 24%. Small interfering RNA-mediated down-regulation of DDAH-1 reduces nitric oxide bioavailability by 27%. The reduction in nitric oxide production following DDAH-1 gene silencing is associated with a 48% reduction in L-Arg/asymmetric dimethylarginine and is partially restored with L-Arg supplementation; overexpression of DDAH-2 increases endothelial nitric oxide by 18%. Small interfering RNA-mediated down-regulation of DDAH-2 reduces nitric oxide bioavailability by 57%. L-Arg and asymmetric dimethylarginine are unchanged in the DDAH-2-silenced cells, and L-Arg supplementation has no effect on nitric oxide
physiological function
results from this animal model of prolonged critical illness show that DDAH activities in several organs in concert determine plasma levels of ADMA, confirming that DDAH is an important player in the regulation of circulatory ADMA
Results 1 - 7 of 7