Variance of DDAH/PRMT/ADMA pathway in atrial fibrillation dogs

Liu, Hongyan; Qu, Xiufen; Liang, Zhaoguang; Chen, Weiye; Song, Ying

doi:10.1016/j.bbrc.2008.10.080

Cited by 21 publications

(20 citation statements)

References 30 publications

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“…However, the question that remains is if the increased ADMA levels are a cause or result in AF? Liu et al demonstrated that AF could increase the expression of protein arginine methyltransferease-1 (PRMT-1), which would lead to an increased ADMA concentration [18], [19]. The previous study also showed that ADMA levels decreased to normal values within 24 hours after AF was terminated by electrical cardioversion.…”

Section: Discussionmentioning

confidence: 97%

Plasma Asymmetric Dimethylarginine and Adverse Events in Patients with Atrial Fibrillation Referred for Coronary Angiogram

Chao

Lin

et al. 2013

PLoS ONE

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ObjectivesElevated plasma levels of asymmetric dimethylarginine (ADMA) have been reported to be associated with endothelial dysfunction, inflammation, and oxidative stress in multiple cardiovascular diseases. This study aimed to investigate whether ADMA was a predictor of clinical outcomes in atrial fibrillation (AF).Methods and ResultsFrom 2006-2009, 990 individuals were referred to our institution for coronary angiography. Among these patients, 141 subjects with a diagnosis of AF, including 52 paroxysmal AF (PAF) and 89 non-paroxysmal AF (non-PAF) patients, were identified as the study population. Plasma ADMA levels were measured. An adverse event was defined as the occurrence of ischemic stroke or cardiovascular death. The ADMA levels were higher in AF than non-AF patients (0.50±0.13 versus 0.45±0.07 µmol/L; p<0.001). Besides, non-PAF patients had higher ADMA levels than PAF patients (0.52±0.15 versus 0.48±0.08 µmol/L; p<0.001). During the follow-up of 30.7±14.4 months, 21 patients (14.9%) experienced adverse events, including cardiovascular death in 7 patients and ischemic stroke in 14. ADMA level, CHA2DS2-VASc score, and left atrial diameter were independent predictors of adverse events in the multivariate analysis. At a cutoff-value of 0.55 µmol/L, the Kaplan-Meier survival analysis showed that patients with a high ADMA level had a higher event rate during the follow-up period.ConclusionsA higher level of ADMA was a risk factor of adverse events in AF patients, which was independent from the CHA2DS2-VASc score. It deserves to further study whether ADMA could potentially refine the clinical risk stratification in AF.

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Section: Discussionmentioning

confidence: 97%

Plasma Asymmetric Dimethylarginine and Adverse Events in Patients with Atrial Fibrillation Referred for Coronary Angiogram

Chao

Lin

et al. 2013

PLoS ONE

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“…Thus, increased ADMA might be one potential factor causing impaired vascular/endothelial function and cardiovascular complications including myocardial infarction and death in patients with AF. However, further prospective clinical studies are warranted to determine if ADMA levels, ADMA degrading enzymes or associated gene polymorphisms can help to predict the prognosis of AF-patients [31].…”

Section: Discussionmentioning

confidence: 99%

The impact of rapid atrial pacing on ADMA and endothelial NOS

Goette

Hammwöhner

Bukowska

et al. 2012

International Journal of Cardiology

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“…Furthermore, the degradation of asymmetrically dimethylated proteins catalyzed by PRMTs produces ADMA, which shows increased circulating levels in numerous diseases (19)(20)(21). Accumulating evidence shows that the deregulated levels of PRMT and its product ADMA may participate in pathogenesis of cancer, viral infections, chronic pulmonary diseases (22), and cardiovascular diseases (23).…”

Section: Discussionmentioning

confidence: 99%

Upregulated Protein Arginine Methyltransferase 1 by IL-4 Increases Eotaxin-1 Expression in Airway Epithelial Cells and Participates in Antigen-Induced Pulmonary Inflammation in Rats

Sun

Yang

Zhong

et al. 2012

The Journal of Immunology

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Protein arginine methyltransferases (PRMTs), catalyzing methylation of both histones and other cellular proteins, have emerged as key regulators of various cellular processes. This study aimed to identify key PRMTs involved in Ag-induced pulmonary inflammation (AIPI), a rat model for asthma, and to explore the role of PRMT1 in the IL-4–induced eosinophil infiltration process. E3 rats were i.p. sensitized with OVA/alum and intranasally challenged with OVA to induce AIPI. The expressions of PRMT1–6, eotaxin-1, and CCR3 in lungs were screened by real-time quantitative PCR. Arginine methyltransferase inhibitor 1 (AMI-1, a pan-PRMT inhibitor) and small interfering RNA–PRMT1 were used to interrupt the function of PRMT1 in A549 cells. In addition, AMI-1 was administrated intranasally to AIPI rats to observe the effects on inflammatory parameters. The results showed that PRMT1 expression was mainly expressed in bronchus and alveolus epithelium and significantly upregulated in lungs from AIPI rats. The inhibition of PRMTs by AMI-1 and the knockdown of PRMT1 expression were able to downregulate the expressions of eotaxin-1 and CCR3 with the IL-4 stimulation in the epithelial cells. Furthermore, AMI-1 administration to AIPI rats can also ameliorate pulmonary inflammation, reduce IL-4 production and humoral immune response, and abrogate eosinophil infiltration into the lungs. In summary, PRMT1 expression is upregulated in AIPI rat lungs and can be stimulated by IL-4. Intervention of PRMT1 activity can abrogate IL-4–dependent eotaxin-1 production to influence the pulmonary inflammation with eosinophil infiltration. The findings may provide experimental evidence that PRMT1 plays an important role in asthma pathogenesis.

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Variance of DDAH/PRMT/ADMA pathway in atrial fibrillation dogs

Cited by 21 publications

References 30 publications

Plasma Asymmetric Dimethylarginine and Adverse Events in Patients with Atrial Fibrillation Referred for Coronary Angiogram

Plasma Asymmetric Dimethylarginine and Adverse Events in Patients with Atrial Fibrillation Referred for Coronary Angiogram

The impact of rapid atrial pacing on ADMA and endothelial NOS

Upregulated Protein Arginine Methyltransferase 1 by IL-4 Increases Eotaxin-1 Expression in Airway Epithelial Cells and Participates in Antigen-Induced Pulmonary Inflammation in Rats

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