Chitosan oligosaccharide ameliorates acute lung injury induced by blast injury through the DDAH1/ADMA pathway

Liu, Yun-En; Tong, Cang-Ci; Zhang, Yu-Biao; Cong, Peifang; Shi, Xiuyun; Liu, Ying; Shi, Lin; Tong, Zhou; Jin, Hongxu; Hou, Mingxiao

doi:10.1371/journal.pone.0192135

Cited by 28 publications

(21 citation statements)

References 38 publications

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“…; Liu et al. ), and DDAH1 upregulation has been associated with tumor regression in a xenograft mouse model (Yung et al. ).…”

Section: Introductionmentioning

confidence: 99%

“…Endothelial DDAH1-specific knockout mice have impaired angiogenesis (Zhang et al 2013;Dowsett et al 2015). DDAH1/ADMA/NOS pathway regulation of caspase-3 mediated apoptosis has been described (Wang et al 2016;Hou et al 2018;Liu et al 2018), and DDAH1 upregulation has been associated with tumor regression in a xenograft mouse model (Yung et al 2016). Caspase-3, in addition to its central role in apoptosis, is paradoxically known to enhance cellular growth (Laplante et al 2010;Li et al 2010;Kennedy et al 2014;Feng et al 2015), and to promote angiogenesis (Povero et al 2013;Feng et al 2015).…”

Section: Introductionmentioning

confidence: 99%

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DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells

et al. 2019

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Nitric Oxide ( NO ) is an endogenous pulmonary vasodilator produced by endothelial NO synthase ( eNOS ). Asymmetric dimethyl L‐arginine ( ADMA ) is an endogenous inhibitor of eNOS activity. In endothelial cells, ADMA is hydrolyzed to L‐citrulline primarily by dimethylarginine dimethyl‐aminohydrolase‐1 ( DDAH 1). We tested the hypothesis that DDAH 1 expression is essential for maintaining NO production in human fetal pulmonary microvascular endothelial cells (hf PMVEC ), such that knockdown of DDAH 1 expression will lead to decreased NO production resulting in less caspase‐3 activation and less tube formation. We found that hf PMVEC transfected with DDAH 1 si RNA had lower NO production than control, with no difference in eNOS protein levels between groups. hf PMVEC transfected with DDAH 1 si RNA had lower protein levels of cleaved caspase‐3 and ‐8 than control. Both DDAH 1 si RNA ‐ and ADMA ‐treated hf PMVEC had greater numbers of viable cells than controls. Angiogenesis was assessed using tube formation assays in matrigel, and tube formation was lower after either DDAH 1 si RNA transfection or ADMA treatment than controls. Addition of an NO donor restored cleaved caspase‐3 and ‐8 protein levels after DDAH 1 si RNA transfection in hf PMVEC to essentially the levels seen in scramble control. Addition of a putative caspase‐3 inhibitor to DDAH 1 si RNA transfected and NO ‐donor treated cells led to greater numbers of viable cells and far less angiogenesis than in any other group studied. We conclude that in hf PMVEC , DDAH 1 is central to the regulation of NO ‐mediated caspase‐3 activation and the resultant apoptosis and angiogenesis. Our findings suggest that DDAH 1 may be a potential therapeutic target in pulmonary hypertensive disorders.

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“…; Liu et al. ), and DDAH1 upregulation has been associated with tumor regression in a xenograft mouse model (Yung et al. ).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells

et al. 2019

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“…Y.‐E. Liu et al () reported that caspase‐3 is a key enzyme that mediates apoptosis. Activated caspase‐3 degrades Bcl‐2 protein to prevent its antiapoptotic effect however, once caspase‐3 is activated, the occurrence of apoptosis is irreversible…”

Section: Discussionmentioning

confidence: 99%

Physiological and structural changes of the lung tissue in male albino rat exposed to immobilization stress

Saber

Aleem

Aziz

et al. 2018

Journal Cellular Physiology

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In case of a life‐threatening, stressful event, the body prepares for an emergency. Indeed, the lung is unique in which alveolar cells are constantly exposed to physical and chemical stresses. This study aimed to study the impact of immobilization stress on the blood–air barrier and how it initiate and maintain an inflammatory response, plus determining the resolution of lung inflammation and repair. There was a significant increase in the plasma levels of stress markers “corticosterone and catecholamines” with a decrease in surfactant protein A (a lung‐injury marker). Chronic stress produced a significant increase in the pulmonary oxidative and inflammatory markers malondialdehyde, tumor necrosis factor α, and induced nitric oxide synthase when compared with that of acute stress. Both stresses provoked marked pulmonary morphological and ultrastructural changes with a significant increase in caspase‐3 immunoexpression. There was increasing evidence of lung’s capacity for repair. This process involved edema resolution, cell proliferation, and tissue remodeling in improving the lung‐injury, oxidative, and inflammatory markers.

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“…A precise model of lung blast injury was used as previously described [10]. Brie y, mice were anesthetized by abdominally injecting 2% pentobarbital sodium (1.5 ml/kg).…”

Section: Blast-exposure Induced Lung Injurymentioning

confidence: 99%

“…Subsequently, intrapulmonary hemorrhage further causes the formation of free radicals, edema, accumulation of in ammatory factors and oxidative damage, which may develop into acute respiratory distress syndrome [9][10][11][12][13]. Our previous studies found that blast injury caused a signi cant increased expression of interleukin-1 (IL-1β), IL-6 and tumor necrosis factor (TNF-α), a signi cant decreased expression of IL-10, an increase in Evans blue leakage, and an signi cant increase in in ammatory cell in ltration [14][15][16]. In addition, we have previously reported that blast exposure-induced in ammation in the lungs occurred within the rst 12-48 h and peaked at approximately 24 h [17].…”

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confidence: 99%

Quantitative proteomic analysis and identification of differentially expressed proteins involved in blast exposure-induced inflammatory response

Liu¹,

Tong

Cong

et al. 2020

Preprint

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Abstract Background Previous studies found that blast injury caused a significant increased expression of interleukin-1, IL-6 and tumor necrosis factor, a significant decrease in the expression of IL-10, an increase in Evans blue leakage, and a significant increase in inflammatory cell infiltration in the lungs. However, the molecular characteristics of lung injury at different time points after blast exposure have not yet been reported. Therefore, in this study, tandem mass spectrometry (TMT) quantitative proteomics and bioinformatics analysis were used for the first time to gain a deeper understanding of the molecular mechanism of lung blast injury at different time points. Methods Fourty-eight male C57BL/6 mice were randomly divided into six groups: control, 12 h, 24 h, 48 h, 72 h and 1 w after low-intensity blast exposure. TMT quantitative proteomics and bioinformatics analysis were performed to analyze protein expression profiling in the lungs from control and blast-exposed mice, and differential protein expression was verified by Western blotting. Results The results demonstrated that blast exposure induced severe lung injury, leukocyte infiltration, and the production of inflammatory factors in mice. After analyzing the expression changes in global proteins and inflammation-related proteomes after blast exposure, the results showed that a total of 6,861 global proteins and 608 differentially expressed proteins were identified, of which 215, 128, 187, 232, and 65 proteins were identified at 12 h, 24 h, 48 h, 72 h, and 1 week after blast exposure, respectively. Moreover, blast exposure-induced 177 differentially expressed proteins were associated with inflammatory responses, which were enriched in the inflammatory response regulation, leukocyte transendothelial migration, phagocytosis, and immune response. Conclusions Therefore, blast exposure may induce early inflammatory response of lung tissue by regulating the expression of key proteins in the inflammatory process, suggesting that early inflammatory response may be the initiating factor of lung blast injury. These data can provide potential therapeutic candidates or approaches for the development of future treatment of lung blast injury.

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Chitosan oligosaccharide ameliorates acute lung injury induced by blast injury through the DDAH1/ADMA pathway

Cited by 28 publications

References 38 publications

DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells

DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells

Physiological and structural changes of the lung tissue in male albino rat exposed to immobilization stress

Quantitative proteomic analysis and identification of differentially expressed proteins involved in blast exposure-induced inflammatory response

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