Dimethylarginine dimethylaminohydrolase (DDAH) overexpression enhances wound repair in airway epithelial cells exposed to agricultural organic dust

Chandra, Deepak; Poole, Jill; Bailey, Kristina L.; Staab, Elizabeth; Sweeter, Jenea M.; DeVasure, Jane M.; Romberger, Debra J.; Wyatt, Todd A.

doi:10.1080/08958378.2018.1474976

Cited by 4 publications

(3 citation statements)

References 42 publications

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“…The damage resulting from DDAH activity can lead to an increased ADMA concentration and a series of reactions, such as severe inflammation and oxidative stress, whereas overexpression of DDAH1 could reduce injury. Chandra et al demonstrated that DDAH1 overexpression could enhance wound repair in agricultural organic dust-treated airway epithelial cells [ 39 ]. Similar results were shown by Kinker et al who found that DDAH1 expression declined in the lung tissue following house dust mite exposure.…”

Section: Discussionmentioning

confidence: 99%

DDAH1 Promotes Lung Endothelial Barrier Repair by Decreasing Leukocyte Transendothelial Migration and Oxidative Stress in Explosion-Induced Lung Injury

Cong

Tong

Mao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Explosion-induced injury is the most commonly encountered wound in modern warfare and incidents. The vascular inflammatory response and subsequent oxidative stress are considered the key causes of morbidity and mortality among those in blast lung injury. It has been reported dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays important roles in regulating vascular endothelial injury repair and angiogenesis, but its role in explosion-induced injury remains to be explained. To explore the mechanism of vascular injury in blast lung, 40 C57BL/6 wild type mice and 40 DDAH1 knockout mice were randomly equally divided into control group and blast group, respectively. Body weight, lung weight, and dry weight of the lungs were recorded. Diffuse vascular leakage was detected by Evans blue test. The serum inflammatory factors, nitric oxide (NO) contents, and ADMA level were determined through ELISA. Hematoxylin-eosin staining and ROS detection were performed for histopathological changes. Western blot was used to detect the proteins related to oxidative stress, cell adhesion molecules and leukocyte transendothelial migration, vascular injury, endothelial barrier dysfunction, and the DDAH1/ADMA/eNOS signaling pathway. We found that DDAH1 deficiency aggravated explosion-induced body weight reduction, lung weight promotion, diffuse vascular leakage histopathological changes, and the increased levels of inflammatory-related factors. Additionally, DDAH1 deficiency also increased ROS generation, MDA, and IRE-1α expression. Regarding vascular endothelial barrier dysfunction, DDAH1 deficiency increased the expression of ICAM-1, Itgal, Rac2, VEGF, MMP9, vimentin, and N-cadherin, while lowering the expression of occludin, CD31, and dystrophin. DDAH1 deficiency also exacerbated explosion-induced increase of ADMA and decrease of eNOS activity and NO contents. Our results indicated that explosion could induce severe lung injury and pulmonary vascular insufficiency, whereas DDAH1 could promote lung endothelial barrier repair and reduce inflammation and oxidative stress by inhibiting ADMA signaling which in turn increased eNOS activity.

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Section: Discussionmentioning

confidence: 99%

DDAH1 Promotes Lung Endothelial Barrier Repair by Decreasing Leukocyte Transendothelial Migration and Oxidative Stress in Explosion-Induced Lung Injury

Cong

Tong

Mao

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…During the normal protein cycle, ADMA is formed enzymatically from the methylation of arginine remnants through the activity of redox-sensitive S-adenosylmethionine-dependent protein arginine N-methyltransferases and metabolized to citrulline by dimethylarginine dimethylaminohydrolase (DDAH) [ 22 ]. ADMA levels reported enhancing during induction of gastric injury with ethanol, indomethacin, cold-stress, and H. pylori [ 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

The effect of Channa striata extract and standard eradication regimen on asymmetric dimethylarginine in Helicobacter pylori gastritis rat model

et al. 2020

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Background and Aim: The presence of gastric mucosa or submucosa inflammation due to Helicobacter pylori leads to histological changes. Gastric injury, pro-inflammatory factors, and oxidative stress in H. pylori infection produce asymmetric dimethylarginine (ADMA), which are a competitive inhibitor of nitric oxide synthase. Investigations were carried out aimed at finding new drugs derived from natural products for the treatment of H. pylori. Channa striata is known to have in vitro anti-inflammatory and antimicrobial properties. This study aimed to investigate the effect of C. striata extract and a standard eradication regimen on ADMA levels and histological changes in the H. pylori gastritis rat model. Materials and Methods: Thirty-five male rats were randomly and equally divided into five groups. Group-1 was the negative control group and Groups-2 to 5 were H. pylori-infected groups. Groups-3 to 5 were administered C. striata extract, a standard eradication regimen, and a combination of standard eradication regimen and C. striata extract, respectively. Histological examination and serum ADMA levels were analyzed. The difference between groups was analyzed using the Kruskal–Wallis and one-way analysis of variance tests. The significance was p<0.05. Results: Serum ADMA levels and severity of gastritis were higher in infected groups compared to the negative control group (p<0.05). The severity of gastritis and mean ADMA levels in the group that received a single administration of the C. striata extract was higher than the others (p<0.05). Serum ADMA levels and severity of gastritis were significantly reduced in the group that received a combination of standard eradication regimen and C. striata extract (p<0.05). Conclusion: Single administration of C. striata extract worsens the severity of gastritis and increased serum ADMA levels in the H. pylori gastritis rat model. The administration of a combination of standard eradication regimen and C. striata extract reduces serum ADMA levels and significantly improves the severity of H. pylori gastritis rat model.

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“…[19]. ADMA выступает в качестве посредника окислительного стресса с помощью подавления eNOS и разобщения путей синтеза NO [20], увеличивая экспрессию воспалительных генов. Выявлено, что в постковидном периоде у пациентов с МС наиболее выраженные (р<0,001) связи между увеличением в сыворотке периферической крови sLIF и уровнями условных вазопрессоров ADMA и SDMA со вторичным снижением вазорелаксанта eNOS, а также повышением функциональных показателей ОПСС и СПВкф.…”

Section: результатыunclassified

Study of Long-Term Clinical and Pathogenetic Effects of Favipiravir-Based Anti-Viral Drug in Patients With Metabolic Syndrome in Post-Covid Period

Radaeva

Балыкова

Zaslavskaya

et al. 2022

Farm. farmakol. (Pâtigorsk)

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The article presents modern scientific data on long-term clinical and pathogenetic effects of the antiviral drug Areplivir (Favipiravir) in patients with metabolic syndrome in the post-COVID period.The aim of the article is to study long-term cytokine-mediated (IL-6/sIL6r and LIF/sLIFr) pathogenetic effects of the favipiravir (Areplivir®) based drug on the incidence of complications in patients with metabolic syndrome in the post-COVID period.Material and methods. With the approval of the local ethics committee at the N.P. Ogarevs Mordovia State University (Protocol No. 5 dated May 17, 2020) “An open prospective comparative study of the Areplivir® (Favipiravir) drug effectiveness in reducing the risk of complications in the post-COVID period in patients with metabolic syndrome” in the Republic of Mordovia was carried out.The study included 190 metabolic syndrome patients who received the outpatient treatment for COVID-19 at Saransk polyclinics from February 2021 to March 2021. The case of COVID-19 was diagnosed in accordance with the current Temporary Guidelines for the prevention, diagnosis and treatment of the new coronavirus infection.Results. The analysis of the metabolic syndrome patients’ follow-up within 1 year after undergoing COVID-19, revealed significant differences in the incidence of complications depending on the intake of the favipiravir based drug. The patients who were administrated with favipiravir at the early stage of infection, were characterized by lower serum levels of four members of the interleukin 6 family – IL-6 (IL-6, sIL6r and LIF, sLIFr) 10, 30 and 180 days after a clinical and laboratory recovery (p<0.001). The average statistical changes in the IL-6 /sIL6r system of the group administrated with favipiravir, were 90%, and they were higher than in the group not administrated with antiviral drugs. In the group of the patients administrated with favipiravir, there was a significant (p<0.001) positive dynamic of the sLIFr indicator, while in the comparison group, there was an increase in this indicator.A protective effect of the early favipiravir use was characterized by a decrease in the frequency of cardiovascular complications, a 2.66-fold decrease in the risk of a stroke and the ACS in the post-COVID period.Conclusion. The areplivir therapy in the acute period of coronavirus infection made it possible to timely reduce the viral load. It helps to correct the pro-inflammatory vector of the immune response at the post-COVID stage and, accordingly, reduces the risk of progression of atherosclerosis, transient cerebrovascular accidents with a cognitive decline, an endothelial dysfunction, and can be considered a secondary prevention of life-threatening cardiovascular complications.

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Dimethylarginine dimethylaminohydrolase (DDAH) overexpression enhances wound repair in airway epithelial cells exposed to agricultural organic dust

Abstract: Preserving the NO signal through endogenous inhibition of asymmetric dimethylarginine enhances wound repair even in the presence of dust exposure.

Cited by 4 publications

References 42 publications

DDAH1 Promotes Lung Endothelial Barrier Repair by Decreasing Leukocyte Transendothelial Migration and Oxidative Stress in Explosion-Induced Lung Injury

DDAH1 Promotes Lung Endothelial Barrier Repair by Decreasing Leukocyte Transendothelial Migration and Oxidative Stress in Explosion-Induced Lung Injury

The effect of Channa striata extract and standard eradication regimen on asymmetric dimethylarginine in Helicobacter pylori gastritis rat model

Study of Long-Term Clinical and Pathogenetic Effects of Favipiravir-Based Anti-Viral Drug in Patients With Metabolic Syndrome in Post-Covid Period

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