Редактирование: DDAH2 (раздел)

==Publications==

{{medline-entry
|title=Epigallocatechin-3-gallate ameliorates erectile function in aged rats via regulation of [[PRMT1]]/DDAH/ADMA/NOS metabolism pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27080477
|abstract=Aging-related ED is predominantly attributed to neurovascular dysfunction mediated by NO suppression and increased oxidative stress in penis. The alterations of protein arginine methyltransferases 1 ([[PRMT1]])/dimethylarginine dimethylaminohydrolase (DDAH)/asymmetrical dimethylarginine (ADMA)/NO synthase (NOS) pathway regulate NO production in the vascular endothelium. Epigallocatechin-3-gallate (EGCG) is one of the most abundant and antioxidative ingredients isolated from green tea. In the present study, 40 Sprague-Dawley rats were randomly distributed into four groups: one young rat group and three aged rat groups treated with daily gavage feedings of EGCG at doses of 0, 10 mg kg-1 and 100 mg kg-1 for 12 weeks, respectively. Erectile function was assessed by electrical stimulation of the cavernous nerves with intracavernous pressure (ICP) measurement. After euthanasia, penile tissue was investigated using Western blot and ELISA to assess the [[PRMT1]]/DDAH/ADMA/NOS metabolism pathway. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were detected by colorimetry. We also evaluated smooth muscle contents. The ratio of maximal ICP and mean systemic arterial pressure (MAP) was markedly higher in EGCG-treated aged rats than in untreated aged rats. We found that [[DDAH1]] and [[DDAH2]] were expressed in cavernosal tissue, and they were downregulated in corpora of aged rats. The administration of EGCG upregulated the expression and activity of DDAH. In contrast, EGCG treatment downregulated the expression of [[PRMT1]] and ADMA content. Moreover, EGCG-treated rats showed an improvement in smooth muscle expression, the ratio of smooth muscle cell/collagen fibril, SOD activity, and MDA levels when compared with untreated aged rats.
|mesh-terms=* Aging
* Amidohydrolases
* Animals
* Antioxidants
* Arginine
* Arterial Pressure
* Catechin
* Cyclic GMP
* Erectile Dysfunction
* Male
* Muscle, Smooth
* Nitric Oxide Synthase
* Penile Erection
* Penis
* Protein-Arginine N-Methyltransferases
* Rats
* Rats, Sprague-Dawley
* Signal Transduction
* Superoxide Dismutase-1

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5427783
}}
{{medline-entry
|title=Regulation of endothelial progenitor cell differentiation and function by dimethylarginine dimethylaminohydrolase 2 in an asymmetric dimethylarginine-independent manner.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24764313
|abstract=Endothelial progenitor cells (EPCs) are involved in the repair of vessels and angiogenesis and are useful in the treatment of ischemic diseases. The dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway is regulated by silent information regulator 1 ([[SIRT1]]), leading to the senescence of endothelial cells (ECs). Here, we demonstrated that peripheral blood EPCs predominantly expressed [[DDAH2]] that increased with EPC differentiation. EPC senescence and dysfunction were induced on interruption of [[DDAH2]] expression, whereas the mRNA expression of vascular endothelial growth factor (VEGF) and kinase-domain insert containing receptor ([[KDR]]) were downregulated. Moreover, [[SIRT1]] expression increased with EPC differentiation. Interruption of [[SIRT1]] inhibited [[DDAH2]], VEGF, and [[KDR]] expression, but had no effect on the level of ADMA. From our data, we concluded that [[DDAH2]] is involved in the differentiation of EPCs and regulates the senescence and function of EPCs through the VEGF/[[KDR]] pathway by activation of [[SIRT1]]. 
|mesh-terms=* Amidohydrolases
* Arginine
* Cell Differentiation
* Cells, Cultured
* Cellular Senescence
* Endothelial Progenitor Cells
* Humans
* RNA Interference
* RNA, Messenger
* RNA, Small Interfering
* Sirtuin 1
* Vascular Endothelial Growth Factor A
* Vascular Endothelial Growth Factor Receptor-2
|keywords=* SIRT1
* dimethylarginine dimethylaminohydrolase
* endothelial progenitor cells
* senescence
|full-text-url=https://sci-hub.do/10.1002/cbin.10288
}}