Log in

Relevant bibliographies by topics / DDAH2 / Journal articles

To see the other types of publications on this topic, follow the link: DDAH2.

Journal articles on the topic 'DDAH2'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'DDAH2.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Kozlova, Alena A., Anastasia N. Vaganova, Roman N. Rodionov, Raul R. Gainetdinov, and Nadine Bernhardt. "Assessment of DDAH1 and DDAH2 Contributions to Psychiatric Disorders via In Silico Methods." International Journal of Molecular Sciences 23, no. 19 (2022): 11902. http://dx.doi.org/10.3390/ijms231911902.

Full text

Abstract:

The contribution of nitric oxide synthases (NOSs) to the pathophysiology of several neuropsychiatric disorders is recognized, but the role of their regulators, dimethylarginine dimethylaminohydrolases (DDAHs), is less understood. This study’s objective was to estimate DDAH1 and DDAH2 associations with biological processes implicated in major psychiatric disorders using publicly accessible expression databases. Since co-expressed genes are more likely to be involved in the same biologic processes, we investigated co-expression patterns with DDAH1 and DDAH2 in the dorsolateral prefrontal cortex

APA, Harvard, Vancouver, ISO, and other styles

2

Dayal, Sanjana, Roman N. Rodionov, Erland Arning, et al. "Tissue-specific downregulation of dimethylarginine dimethylaminohydrolase in hyperhomocysteinemia." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (2008): H816—H825. http://dx.doi.org/10.1152/ajpheart.01348.2007.

Full text

Abstract:

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, has been proposed to be a mediator of vascular dysfunction during hyperhomocysteinemia. Levels of ADMA are regulated by dimethylarginine dimethylaminohydrolase (DDAH). Using both in vitro and in vivo approaches, we tested the hypothesis that hyperhomocysteinemia causes downregulation of the two genes encoding DDAH ( Ddah1 and Ddah2). In the MS-1 murine endothelial cell line, the addition of homocysteine decreased NO production but did not elevate ADMA or alter levels of Ddah1 or Ddah2 mRNA. Mice heterozy

APA, Harvard, Vancouver, ISO, and other styles

3

Ivashchenko, Christine Y., Benjamin T. Bradley, Zhaohui Ao, James Leiper, Patrick Vallance, and Douglas G. Johns. "Regulation of the ADMA-DDAH system in endothelial cells: a novel mechanism for the sterol response element binding proteins, SREBP1c and -2." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (2010): H251—H258. http://dx.doi.org/10.1152/ajpheart.00195.2009.

Full text

Abstract:

Asymmetric dimethylarginine (ADMA) has been implicated in the progression of cardiovascular disease as an endogenous inhibitor of nitric oxide synthase. The regulation of dimethylarginine dimethylaminohydrolase (DDAH), the enzyme responsible for metabolizing ADMA, is poorly understood. The transcription factor sterol response element binding protein (SREBP) is activated by statins via a reduction of membrane cholesterol content. Because the promoters of both DDAH1 and DDAH2 isoforms contain sterol response elements, we tested the hypothesis that simvastatin regulates DDAH1 and DDAH2 transcript

APA, Harvard, Vancouver, ISO, and other styles

4

Sasaki, Akihito, Shouzaburoh Doi, Shuki Mizutani, and Hiroshi Azuma. "Roles of accumulated endogenous nitric oxide synthase inhibitors, enhanced arginase activity, and attenuated nitric oxide synthase activity in endothelial cells for pulmonary hypertension in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 6 (2007): L1480—L1487. http://dx.doi.org/10.1152/ajplung.00360.2006.

Full text

Abstract:

Nitric oxide (NO) has been suggested to play a key role in the pathogenesis of pulmonary hypertension (PH). To determine which mechanism exists to affect NO production, we examined the concentration of endogenous nitric oxide synthase (NOS) inhibitors and their catabolizing enzyme dimethylarginine dimethylaminohydrolase (DDAH) activity and protein expression (DDAH1 and DDAH2) in pulmonary artery endothelial cells (PAECs) of rats given monocrotaline (MCT). We also measured NOS and arginase activities and NOS protein expression. Twenty-four days after MCT administration, PH and right ventricle (

APA, Harvard, Vancouver, ISO, and other styles

5

Hannemann, Juliane, Patricia Siques, Lena Schmidt-Hutten, Julia Zummack, Julio Brito, and Rainer Böger. "Association of Genes of the NO Pathway with Altitude Disease and Hypoxic Pulmonary Hypertension." Journal of Clinical Medicine 10, no. 24 (2021): 5761. http://dx.doi.org/10.3390/jcm10245761.

Full text

Abstract:

Chronic intermittent hypoxia leads to high-altitude pulmonary hypertension, which is associated with high asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthesis. Therefore, we aimed to understand the relation of single nucleotide polymorphisms in this pathway to high-altitude pulmonary hypertension (HAPH). We genotyped 69 healthy male Chileans subjected to chronic intermittent hypoxia. Acclimatization to altitude was determined using the Lake Louise Score and the presence of acute mountain sickness. Echocardiography was performed after six months in 24 individual

APA, Harvard, Vancouver, ISO, and other styles

6

Krzystek-Korpacka, Małgorzata, Berenika Szczęśniak-Sięga, Izabela Szczuka, et al. "L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs." Cancers 12, no. 9 (2020): 2594. http://dx.doi.org/10.3390/cancers12092594.

Full text

Abstract:

L-arginine/nitric oxide pathway metabolites are altered in colorectal cancer (CRC). We evaluated underlying changes in pathway enzymes in 55 paired tumor/tumor-adjacent samples and 20 normal mucosa using quantitative-PCR and assessed the impact of classic and novel oxicam analogues on enzyme expression and intracellular metabolite concentration (LC-MS/MS) in Caco-2, HCT116, and HT-29 cells. Compared to normal mucosa, ARG1, PRMT1, and PRMT5 were overexpressed in both tumor and tumor-adjacent tissue and DDAH2 solely in tumor-adjacent tissue. Tumor-adjacent tissue had higher expression of ARG1, D

APA, Harvard, Vancouver, ISO, and other styles

7

Hannemann, Juliane, Julia Zummack, Jonas Hillig, Leonard Rendant-Gantzberg, and Rainer Böger. "Association of Variability in the DDAH1, DDAH2, AGXT2 and PRMT1 Genes with Circulating ADMA Concentration in Human Whole Blood." Journal of Clinical Medicine 11, no. 4 (2022): 941. http://dx.doi.org/10.3390/jcm11040941.

Full text

Abstract:

Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthesis and a cardiovascular risk factor. Its regulation has been studied extensively in experimental models, but less in humans. We studied common single-nucleotide polymorphisms (SNPs) in genes encoding for enzymes involved in ADMA biosynthesis and metabolism, i.e., PRMT1, DDAH1, DDAH2, and AGXT2, and assessed their associations with blood ADMA concentration in 377 unselected humans. The minor allele of DDAH1 SNP rs233112 was significantly more frequent in individuals with ADMA in the highest tertile or in the highest q

APA, Harvard, Vancouver, ISO, and other styles

8

Wang, Zhong, Shaoze Chen, Lina Zhang, et al. "Association between variation in the genes DDAH1 and DDAH2 and hypertension among Uygur, Kazakh and Han ethnic groups in China." Sao Paulo Medical Journal 134, no. 3 (2016): 205–10. http://dx.doi.org/10.1590/1516-3180.2015.01150108.

Full text

Abstract:

CONTEXT AND OBJECTIVE: Dimethylarginine dimethylaminohydrolase enzymes (DDAH), which are encoded by the genes DDAH1 and DDAH2, play a fundamental role in maintaining endothelial function. We conducted a case-control study on a Chinese population that included three ethnic groups (Han, Kazakh and Uygur), to systemically investigate associations between variations in the genes DDAH1 and DDAH2 and hypertension. DESIGN AND SETTING: Experimental study at the Department of Internal Medicine and Genetic Diagnosis, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology.

APA, Harvard, Vancouver, ISO, and other styles

9

Krzystek-Korpacka, Małgorzata, Mariusz G. Fleszar, Iwona Bednarz-Misa, et al. "Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings." International Journal of Molecular Sciences 21, no. 5 (2020): 1641. http://dx.doi.org/10.3390/ijms21051641.

Full text

Abstract:

L-arginine/nitric oxide pathway in Crohn’s disease (CD) and ulcerative colitis (UC) is poorly investigated. The aim of current study is to quantify pathway serum metabolites in 52 CD (40 active), 48 UC (33 active), and 18 irritable bowel syndrome patients and 40 controls using mass spectrometry and at determining mRNA expression of pathway-associated enzymes in 91 bowel samples. Arginine and symmetric dimethylarginine decreased (p < 0.05) in active-CD (129 and 0.437 µM) compared to controls (157 and 0.494 µM) and active-UC (164 and 0.52 µM). Citrulline and dimethylamine increased (p < 0.

APA, Harvard, Vancouver, ISO, and other styles

10

Jarzebska, Natalia, Arduino A. Mangoni, Jens Martens-Lobenhoffer, Stefanie M. Bode-Böger, and Roman N. Rodionov. "The Second Life of Methylarginines as Cardiovascular Targets." International Journal of Molecular Sciences 20, no. 18 (2019): 4592. http://dx.doi.org/10.3390/ijms20184592.

Full text

Abstract:

Endogenous methylarginines were proposed as cardiovascular risk factors more than two decades ago, however, so far, this knowledge has not led to the development of novel therapeutic approaches. The initial studies were primarily focused on the endogenous inhibitors of nitric oxide synthases asymmetric dimethylarginine (ADMA) and monomethylarginine (MMA) and the main enzyme regulating their clearance dimethylarginine dimethylaminohydrolase 1 (DDAH1). To date, all the screens for DDAH1 activators performed with the purified recombinant DDAH1 enzyme have not yielded any promising hits, which is

APA, Harvard, Vancouver, ISO, and other styles

11

Hannemann, Juliane, Leticia Oliveira Ferrer, Antonia Röglin, et al. "Abstract 7660: L-Arginine metabolism is of prognostic relevance in women with breast cancer, but varies considerably between subtypes in vitro - A bedside-to-bench translational approach." Cancer Research 84, no. 6_Supplement (2024): 7660. http://dx.doi.org/10.1158/1538-7445.am2024-7660.

Full text

Abstract:

Abstract Availability of the semi-essential amino acid L-arginine (L-arg) is limiting for proliferation in highly proliferative tissues. L-Arg is also a substrate for nitric oxide synthases (NOS) and arginases (ARG) 1 and 2. Methylation of L-arg residues within proteins by protein L-arg methyltransferases (PRMTs) leads to asymmetric (ADMA) and symmetric dimethylarginine (SDMA). Protein L-arg methylation is an important post-translational mechanism to regulate gene expression and cell cycle control. We measured L-arg and its metabolites in a prospective cohort of patients with primary breast ca

APA, Harvard, Vancouver, ISO, and other styles

12

Redel, Bethany K., Kimberly J. Tessanne, Lee D. Spate, Clifton N. Murphy, and Randall S. Prather. "Arginine increases development of in vitro-produced porcine embryos and affects the protein arginine methyltransferase–dimethylarginine dimethylaminohydrolase–nitric oxide axis." Reproduction, Fertility and Development 27, no. 4 (2015): 655. http://dx.doi.org/10.1071/rd14293.

Full text

Abstract:

Culture systems promote development at rates lower than the in vivo environment. Here, we evaluated the embryo’s transcriptome to determine what the embryo needs during development. A previous mRNA sequencing endeavour found upregulation of solute carrier family 7 (cationic amino acid transporter, y+ system), member 1 (SLC7A1), an arginine transporter, in in vitro- compared with in vivo-cultured embryos. In the present study, we added different concentrations of arginine to our culture medium to meet the needs of the porcine embryo. Increasing arginine from 0.12 to 1.69 mM improved the number

APA, Harvard, Vancouver, ISO, and other styles

13

Huang, Shan, Zexing Li, Zewen Wu, et al. "DDAH2 suppresses RLR-MAVS–mediated innate antiviral immunity by stimulating nitric oxide–activated, Drp1-induced mitochondrial fission." Science Signaling 14, no. 678 (2021): eabc7931. http://dx.doi.org/10.1126/scisignal.abc7931.

Full text

Abstract:

The RIG-I–like receptor (RLR) signaling pathway is pivotal for innate immunity against invading viruses, and dysregulation of this molecular cascade has been linked to various diseases. Here, we identified dimethylarginine dimethylaminohydrolase 2 (DDAH2) as a potent regulator of the RLR-mediated antiviral response in human and mouse. Overexpression of DDAH2 attenuated RLR signaling, whereas loss of DDAH2 function enhanced RLR signaling and suppressed viral replication ex vivo and in mice. Upon viral infection, DDAH2 relocated to mitochondria, where it induced the production of nitric oxide (N

APA, Harvard, Vancouver, ISO, and other styles

14

Jia, Su-Jie, Kui Song, Guang-Ping Wang, et al. "Regulation by DDAH/ADMA pathway of lipopolysaccharideinduced tissue factor expression in endothelial cells." Thrombosis and Haemostasis 97, no. 05 (2007): 830–38. http://dx.doi.org/10.1160/th06-11-0656.

Full text

Abstract:

SummaryPrevious studies have shown the regulatory effect of nitric oxide (NO) on endotoxin-induced tissue factor (TF) in endothelial cells. Asymmetric dimethylarginine (ADMA), a major endogenous NO synthase (NOS) inhibitor, could inhibit NO production in vivo and in vitro. ADMA and its major hydrolase dimethylarginine dimethylaminohydrolase (DDAH) have recently been thought of as a novel regulatory system of endogenous NO production. The aim of the present study was to determine whether the DDAH/ADMA pathway is involved in the effect of lipopolysaccharide (LPS) on TF expression in endothelial

APA, Harvard, Vancouver, ISO, and other styles

15

Bai, Yongyi, Jingzhou Chen, Kai Sun, Ying Xin, Junhao Liu, and Rutai Hui. "Common genetic variation in DDAH2 is associated with intracerebral haemorrhage in a Chinese population: a multi-centre case-control study in China." Clinical Science 117, no. 7 (2009): 273–79. http://dx.doi.org/10.1042/cs20090005.

Full text

Abstract:

ADMA (asymmetric ω-NG,NG-dimethylarginine), an endogenous inhibitor of NOS (NO synthase), has been shown to be an independent predictor of cerebrovascular disorders. DDAH2 (dimethylarginine dimethylaminohydrolase 2) promotes the metabolism of ADMA and plays a key role in the regulation of the acute inflammatory response. We hypothesized that genetic variation in DDAH2 might alter the susceptibility to ICH (intracerebral haemorrhage). The hypothesis was tested in two independent case-control studies. We used a haplotype-tagging SNP (single nucleotide polymorphism) approach to identify tag SNPs

APA, Harvard, Vancouver, ISO, and other styles

16

Puchau, Blanca, Helen Hermana M. Hermsdorff, M. Ángeles Zulet, and J. Alfredo Martínez. "DDAH2 mRNA Expression Is Inversely Associated with Some Cardiovascular Risk-Related Features in Healthy Young Adults." Disease Markers 27, no. 1 (2009): 37–44. http://dx.doi.org/10.1155/2009/978157.

Full text

Abstract:

The purpose of this study was to evaluate whether the mRNA expression profiles of three genes (PRMT1, DDAH2 and NOS3) are related to ADMA metabolism and signalling, and the potential relationships with anthropometrical, biochemical, lifestyle and inflammatory indicators in healthy young adults. An emphasis on the putative effect of different mRNA expression on cardiovascular risk-related features was paid. Anthropometrical measurements as well as lifestyle features were analyzed in 120 healthy young adults. Fasting blood samples were collected for the measurement of glucose and lipid profiles

APA, Harvard, Vancouver, ISO, and other styles

17

Jacobi, Johannes, Renke Maas, Nada Cordasic, et al. "Role of asymmetric dimethylarginine for angiotensin II-induced target organ damage in mice." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (2008): H1058—H1066. http://dx.doi.org/10.1152/ajpheart.01103.2007.

Full text

Abstract:

The aim of the present study was to investigate the role of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) and its degrading enzyme dimethylarginine dimethylaminohydrolase (DDAH) in angiotensin II (ANG II)-induced hypertension and target organ damage in mice. Mice transgenic for the human DDAH1 gene (TG) and wild-type (WT) mice (each, n = 28) were treated with 1.0 μg·kg−1·min−1 ANG II, 3.0 μg·kg−1·min−1 ANG II, or phosphate-buffered saline over 4 wk via osmotic minipumps. Blood pressure, as measured by tail cuff, was elevated to the same degree in TG and WT m

APA, Harvard, Vancouver, ISO, and other styles

18

Khor, G. H., G. R. A. Froemming, R. B. Zain, et al. "DNA Methylation Profiling Revealed Promoter Hypermethylation-induced Silencing of p16, DDAH2 and DUSP1 in Primary Oral Squamous Cell Carcinoma." International Journal of Medical Sciences 10, no. 12 (2014): 1727–39. https://doi.org/10.7150/ijms.6884.

Full text

Abstract:

Background: Hypermethylation in promoter regions of genes might lead to altered gene functions and result in malignant cellular transformation. Thus, biomarker identification for hypermethylated genes would be very useful for early diagnosis, prognosis, and therapeutic treatment of oral squamous cell carcinoma (OSCC). The objectives of this study were to screen and validate differentially hypermethylated genes in OSCC and correlate the hypermethylation-induced genes with demographic, clinocopathological characteristics and survival rate of OSCC. Methods: DNA methylation profiling was utilized

APA, Harvard, Vancouver, ISO, and other styles

19

Hannemann, Juliane, Daniel Appel, Miriam Seeberger-Steinmeister, Tabea Brüning, Julia Zummack, and Rainer Böger. "Sequence Variation in the DDAH1 Gene Predisposes for Delayed Cerebral Ischemia in Subarachnoidal Hemorrhage." Journal of Clinical Medicine 9, no. 12 (2020): 3900. http://dx.doi.org/10.3390/jcm9123900.

Full text

Abstract:

Delayed cerebral ischemia (DCI) often causes poor long-term neurological outcome after subarachnoidal hemorrhage (SAH). Asymmetric dimethylarginine (ADMA) inhibits nitric oxide synthase (NOS) and is associated with DCI after SAH. We studied single nucleotide polymorphisms (SNPs) in the NOS3, DDAH1, DDAH2, PRMT1, and AGXT2 genes that are part of the L-arginine–ADMA–NO pathway, and their association with DCI. We measured L-arginine, ADMA and symmetric dimethylarginine (SDMA) in plasma and cerebrospinal fluid (CSF) of 51 SAH patients at admission; follow-up was until 30 days post-discharge. The p

APA, Harvard, Vancouver, ISO, and other styles

20

Tessanne, K., B. Redel, K. Whitworth, L. Spate, A. Brown, and R. S. Prather. "145 CHARACTERIZATION OF THE PROTEIN ARGININE METHYLTRANSFERASE-DIMETHYLARGININE DIMETHYLAMINOHYDROLASE-NITRIC OXIDE AXIS DURING PORCINE EMBRYO DEVELOPMENT." Reproduction, Fertility and Development 24, no. 1 (2012): 185. http://dx.doi.org/10.1071/rdv24n1ab145.

Full text

Abstract:

Transcriptional deep sequencing analysis by Bauer et al. (2010) revealed a significant increase in expression of the arginine transporter SLC7A1 in in vitro–cultured porcine blastocysts compared with those cultured in vivo and this was corrected through supplemental arginine. This indicates an important role for arginine during porcine embryo development. Arginine is the precursor for nitric oxide (NO) production and previous work in mice and cattle has shown decreased development when embryos were cultured with a nitric oxide synthase (NOS) inhibitor. The NOS activity is inhibited by monometh

APA, Harvard, Vancouver, ISO, and other styles

21

Tran, Cam T. L., Margaret F. Fox, Patrick Vallance, and James M. Leiper. "Chromosomal Localization, Gene Structure, and Expression Pattern of DDAH1: Comparison with DDAH2 and Implications for Evolutionary Origins." Genomics 68, no. 1 (2000): 101–5. http://dx.doi.org/10.1006/geno.2000.6262.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Liu, Li-Hua, Zheng Guo, Mei Feng, Zhong-Zu Wu, Zhi-Min He, and Yan Xiong. "Protection of DDAH2 Overexpression Against Homocysteine-Induced Impairments of DDAH/ADMA/NOS/NO Pathway in Endothelial Cells." Cellular Physiology and Biochemistry 30, no. 6 (2012): 1413–22. http://dx.doi.org/10.1159/000343329.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Lumicisi, B. A., J. E. Cartwright, K. Leslie, A. E. Wallace, and G. S. Whitley. "Inhibition of DDAH1, but not DDAH2, results in apoptosis of a human trophoblast cell line in response to TRAIL." Human Reproduction 30, no. 8 (2015): 1813–19. http://dx.doi.org/10.1093/humrep/dev138.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Brites-Anselmi, Guilhermo, Ana Maria Milanez Azevedo, Anderson Heiji Lima Miyazaki, et al. "DDAH1 and DDAH2 polymorphisms associate with asymmetrical dimethylarginine plasma levels in erectile dysfunction patients but not in healthy controls." Nitric Oxide 92 (November 2019): 11–17. http://dx.doi.org/10.1016/j.niox.2019.08.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

GAD, MOHAMED Z., SALLY I. HASSANEIN, SAHAR M. ABDEL-MAKSOUD, GAMAL M. SHABAN, and KHALED ABOU-AISHA. "Association of DDAH2 gene polymorphism with cardiovascular disease in Egyptian patients." Journal of Genetics 90, no. 1 (2011): 161–63. http://dx.doi.org/10.1007/s12041-011-0043-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Rodríguez-Pérez, José Manuel, Nonanzit Pérez-Hernández, Rocío Arellano-Zapoteco, et al. "PROTECTIVE ROLE OF DDAH2 GENE HAPLOTYPES IN PATIENTS WITH MYOCARDIAL INFARCTION." Journal of the American College of Cardiology 61, no. 10 (2013): E165. http://dx.doi.org/10.1016/s0735-1097(13)60166-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Abhary, Sotoodeh, Kathryn P. Burdon, Abraham Kuot, et al. "Sequence Variation in DDAH1 and DDAH2 Genes Is Strongly and Additively Associated with Serum ADMA Concentrations in Individuals with Type 2 Diabetes." PLoS ONE 5, no. 3 (2010): e9462. http://dx.doi.org/10.1371/journal.pone.0009462.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Pérez-Hernández, Nonanzit, Gilberto Vargas-Alarcón, Rocio Arellano-Zapoteco, et al. "Protective role of DDAH2 (rs805304) gene polymorphism in patients with myocardial infarction." Experimental and Molecular Pathology 97, no. 3 (2014): 393–98. http://dx.doi.org/10.1016/j.yexmp.2014.09.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Seo, Hyun-Ae, Su-Won Kim, Eon-Ju Jeon, et al. "Association of the DDAH2 gene polymorphism with type 2 diabetes and hypertension." Diabetes Research and Clinical Practice 98, no. 1 (2012): 125–31. http://dx.doi.org/10.1016/j.diabres.2012.04.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Hannemann, Juliane, Julia Zummack, Jonas Hillig, and Rainer Böger. "Metabolism of asymmetric dimethylarginine in hypoxia: from bench to bedside." Pulmonary Circulation 10, no. 1_suppl (2020): 31–41. http://dx.doi.org/10.1177/2045894020918846.

Full text

Abstract:

Acute hypoxia and chronic hypoxia induce pulmonary vasoconstriction. While hypoxic pulmonary vasoconstriction is a physiological response if parts of the lung are affected, global exposure to hypoxic conditions may lead to clinical conditions like high-altitude pulmonary hypertension. Nitric oxide is the major vasodilator released from the vascular endothelium. Nitric oxide-dependent vasodilation is impaired in hypoxic conditions. Inhibition of nitric oxide synthesis is the most rapid and easily reversible molecular mechanism to regulate nitric oxide-dependent vascular function in response to

APA, Harvard, Vancouver, ISO, and other styles

31

Chen, Weixia, Huiqin Wang, Jing Liu, and Kaixia Li. "Interference of KLF9 relieved the development of gestational diabetes mellitus by upregulating DDAH2." Bioengineered 13, no. 1 (2021): 395–406. http://dx.doi.org/10.1080/21655979.2021.2005929.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Feng, Jinzhong, Hede Luo, Yihua Qiu, Wei Zhou, Feng Yu, and Feng Wu. "Down-regulation of DDAH2 and eNOS induces endothelial dysfunction in sinoaortic-denervated rats." European Journal of Pharmacology 661, no. 1-3 (2011): 86–91. http://dx.doi.org/10.1016/j.ejphar.2011.04.041.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Jung, Carla S., Brian A. Iuliano, Judith Harvey-White, Michael G. Espey, Edward H. Oldfield, and Ryszard M. Pluta. "Association between cerebrospinal fluid levels of asymmetric dimethyl-L-arginine, an endogenous inhibitor of endothelial nitric oxide synthase, and cerebral vasospasm in a primate model of subarachnoid hemorrhage." Journal of Neurosurgery 101, no. 5 (2004): 836–42. http://dx.doi.org/10.3171/jns.2004.101.5.0836.

Full text

Abstract:

Object. Decreased availability of nitric oxide (NO) has been proposed to evoke delayed cerebral vasospasm after subarachnoid hemorrhage (SAH). Asymmetric dimethyl-l-arginine (ADMA) inhibits endothelial NO synthase (eNOS) and, therefore, may be responsible for decreased NO availability in cases of cerebral vasospasm. The goal of this study was to determine whether ADMA levels are associated with cerebral vasospasm in a primate model of SAH. Methods. Twenty-two cynomolgus monkeys (six control animals and 16 with SAH) were used in this study. The levels of ADMA, l-arginine, l-citrulline, nitrites

APA, Harvard, Vancouver, ISO, and other styles

34

Jones, L. C., C. T. L. Tran, J. M. Leiper, A. D. Hingorani, and P. Vallance. "Common genetic variation in a basal promoter element alters DDAH2 expression in endothelial cells." Biochemical and Biophysical Research Communications 310, no. 3 (2003): 836–43. http://dx.doi.org/10.1016/j.bbrc.2003.09.097.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Lee, WY, SY Chai, KH Lee, et al. "Identification of the DDAH2 Protein in Pig Reproductive Tract Mucus: A Putative Oestrus Detection Marker." Reproduction in Domestic Animals 48, no. 1 (2012): e13-e16. http://dx.doi.org/10.1111/j.1439-0531.2012.02122.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Hultström, Michael, Frank Helle, and Bjarne M. Iversen. "AT1 receptor activation regulates the mRNA expression of CAT1, CAT2, arginase-1, and DDAH2 in preglomerular vessels from angiotensin II hypertensive rats." American Journal of Physiology-Renal Physiology 297, no. 1 (2009): F163—F168. http://dx.doi.org/10.1152/ajprenal.00087.2009.

Full text

Abstract:

Previously, we found increased expression of l-arginine metabolizing enzymes in both kidneys from two-kidney, one-clip (2K1C) hypertensive rats (Helle F, Hultstrom M, Skogstrand T, Palm F, Iversen BM. Am J Physiol Renal Physiol 296: F78–F86, 2009). In the present study, we investigate whether AT1 receptor activation can induce the changes observed in 2K1C. Four groups of rats were infused with 80 ng/min ANG II or saline for 14 days and/or given 60 mg·kg−1·day−1 losartan. Gene expression was studied in isolated preglomerular vessels by RT-PCR. Dose-responses to ANG II were studied in isolated p

APA, Harvard, Vancouver, ISO, and other styles

37

Zhang, Bi-Kui, Yong-Quan Lai, Pan-Pan Niu, Ming Zhao, and Su-Jie Jia. "Epigallocatechin-3-Gallate Inhibits Homocysteine-Induced Apoptosis of Endothelial Cells by Demethylation of the DDAH2 Gene." Planta Medica 79, no. 18 (2013): 1715–19. http://dx.doi.org/10.1055/s-0033-1351017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Garbin, Ulisse, Anna Fratta Pasini, Chiara Stranieri, Stefania Manfro, Veronica Boccioletti, and Luciano Cominacini. "Nebivolol reduces asymmetric dimethylarginine in endothelial cells by increasing dimethylarginine dimethylaminohydrolase 2 (DDAH2) expression and activity." Pharmacological Research 56, no. 6 (2007): 515–21. http://dx.doi.org/10.1016/j.phrs.2007.09.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Cillero-Pastor, B., J. Mateos, C. Ruiz-Romero, and F. J. Blanco. "187 IL-1BETA TRANSLOCATES THE PROTEIN DIMETHYLARGININASE 2 (DDAH2) TO THE MITOCHONDRION OF HUMAN NORMAL CHONDROCYTES." Osteoarthritis and Cartilage 18 (October 2010): S90. http://dx.doi.org/10.1016/s1063-4584(10)60214-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Wojciak-Stothard, Beata, Belen Torondel, Lan Zhao, Thomas Renné, and James M. Leiper. "Modulation of Rac1 Activity by ADMA/DDAH Regulates Pulmonary Endothelial Barrier Function." Molecular Biology of the Cell 20, no. 1 (2009): 33–42. http://dx.doi.org/10.1091/mbc.e08-04-0395.

Full text

Abstract:

Endogenously produced nitric oxide synthase inhibitor, asymmetric methylarginine (ADMA) is associated with vascular dysfunction and endothelial leakage. We studied the role of ADMA, and the enzymes metabolizing it, dimethylarginine dimethylaminohydrolases (DDAH) in the regulation of endothelial barrier function in pulmonary macrovascular and microvascular cells in vitro and in lungs of genetically modified heterozygous DDAHI knockout mice in vivo. We show that ADMA increases pulmonary endothelial permeability in vitro and in in vivo and that this effect is mediated by nitric oxide (NO) acting

APA, Harvard, Vancouver, ISO, and other styles

41

Niu, Pan-Pan, Yu Cao, Ting Gong, Jin-Hui Guo, Bi-Kui Zhang, and Su-Jie Jia. "Hypermethylation of DDAH2 promoter contributes to the dysfunction of endothelial progenitor cells in coronary artery disease patients." Journal of Translational Medicine 12, no. 1 (2014): 170. http://dx.doi.org/10.1186/1479-5876-12-170.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Marra, Maurizio, Francesca Marchegiani, Antonio Ceriello, et al. "Chronic renal impairment and DDAH2-1151 A/C polymorphism determine ADMA levels in type 2 diabetic subjects." Nephrology Dialysis Transplantation 28, no. 4 (2012): 964–71. http://dx.doi.org/10.1093/ndt/gfs516.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Xiao, Hong-Bo, Guo-Guang Sui, Xiang-Yang Lu, and Zhi-Liang Sun. "Elevated Levels of ADMA Are Associated with Lower DDAH2 and Higher PRMT1 in LPS-Induced Endometritis Rats." Inflammation 41, no. 1 (2017): 299–306. http://dx.doi.org/10.1007/s10753-017-0687-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

ZHANG, Jing-ge, Jun-xu LIU, Zhu-hua LI, Li-zhen WANG, Yi-deng JIANG, and Shu-ren WANG. "Dysfunction of endothelial NO system originated from homocysteine-induced aberrant methylation pattern in promoter region of DDAH2 gene." Chinese Medical Journal 120, no. 23 (2007): 2132–37. http://dx.doi.org/10.1097/00029330-200712010-00013.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Khor, Goot Heah, Gabriele Ruth Anisah Froemming, Rosnah Binti Zain, et al. "DNA Methylation Profiling Revealed Promoter Hypermethylation-induced Silencing of p16, DDAH2 and DUSP1 in Primary Oral Squamous Cell Carcinoma." International Journal of Medical Sciences 10, no. 12 (2013): 1727–39. http://dx.doi.org/10.7150/ijms.6884.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Hasegawa, Kazuhiro, Shu Wakino, Masumi Kimoto, et al. "The hydrolase DDAH2 enhances pancreatic insulin secretion by transcriptional regulation of secretagogin through a Sirt1‐dependent mechanism in mice." FASEB Journal 27, no. 6 (2013): 2301–15. http://dx.doi.org/10.1096/fj.12-226092.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Weiss, Scott L., Min Yu, Lawrence Jennings, Shannon Haymond, Gang Zhang, and Mark S. Wainwright. "Pilot Study of the Association of the DDAH2 −449G Polymorphism with Asymmetric Dimethylarginine and Hemodynamic Shock in Pediatric Sepsis." PLoS ONE 7, no. 3 (2012): e33355. http://dx.doi.org/10.1371/journal.pone.0033355.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Zhou, Yi-ming, Xi Lan, Han-bin Guo, Yan Zhang, Li Ma, and Jian-biao Cao. "Rho/ROCK Signal Cascade Mediates Asymmetric Dimethylarginine-Induced Vascular Smooth Muscle Cells Migration and Phenotype Change." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/683707.

Full text

Abstract:

Asymmetric dimethylarginine (ADMA) induces vascular smooth muscle cells (VSMCs) migration. VSMC phenotype change is a prerequisite of migration. RhoA and Rho-kinase (ROCK) mediate migration of VSMCs. We hypothesize that ADMA induces VSMC migration via the activation of Rho/ROCK signal pathway and due to VSMCs phenotype change. ADMA activates Rho/ROCK signal pathway that interpreted by the elevation of RhoA activity and phosphorylation level of a ROCK substrate. Pretreatment with ROCK inhibitor, Y27632 completely reverses the induction of ADMA on ROCK and in turn inhibits ADMA-induced VSMCs mig

APA, Harvard, Vancouver, ISO, and other styles

49

Bäckdahl, Liselotte, Marlis Herberth, Gareth Wilson, et al. "Gene body methylation of the dimethylarginine dimethylamino-hydrolase 2 (Ddah2) gene is an epigenetic biomarker for neural stem cell differentiation." Epigenetics 4, no. 4 (2009): 248–54. http://dx.doi.org/10.4161/epi.9093.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Kelly, Peter, Zhen Wang, Blerina Ahmetaj, et al. "Dimethylarginine dimethylaminohydrolase 2 (DDAH2) regulates nitric oxide production, haemodynamics and vascular responsiveness under basal conditions and outcome in polymicrobial sepsis." Nitric Oxide 42 (November 2014): 130. http://dx.doi.org/10.1016/j.niox.2014.09.094.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!