Role of MAPK/AP-1 signaling pathway in the protection of CEES-induced lung injury by antioxidant liposome

Mukhopadhyay, Sutapa; Mukherjee, Sanjoy; Stone, William L.; Smith, Milton; Das, Salil K.

doi:10.1016/j.tox.2009.05.010

Cited by 40 publications

(29 citation statements)

References 33 publications

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“…For example, Trolox, a water-soluble analog of α-tocopherol (vitamin E) has been reported to reduce markers of oxidative damage induced by SM in rodents (Kumar et al, 2001), although inflammatory markers were not affected (Anderson et al, 2009). Liposomes containing tocopherols, alone or in combination with NAC, were also found to suppress CEES-induced lung inflammation and injury (Hoesel et al, 2008; Mukherjee et al, 2009; Mukhopadhyay et al, 2009). Liposomes containing both NAC and tocopherols appear to be more effective in reducing collagen deposition in the chronic injury phase induced by CEES than those containing either agent alone (Hoesel et al, 2008; Mukherjee et al, 2009).…”

Section: Targeting Reactive Oxygen and Nitrogen Speciesmentioning

confidence: 99%

“…Administration of NAC as late as 90 min after CEES exposure significantly reduces acute lung injury in rats (Das et al, 2003; McClintock et al, 2002). Similarly, treatment of rats with NAC-containing liposomes immediately or up to one hour after CEES reduces both lung permeability and BAL levels of pro-inflammatory cytokines including IL-1, IL-6, TNFα, and CXCL1 (Hoesel et al, 2008; McClintock et al, 2006; Mukherjee et al, 2009); this was associated with down regulation of the AP-1 transcription factor, which is important in regulating inflammatory gene expression (Mukhopadhyay et al, 2009). In a more recent study in pigs, treatment with multiple doses of NAC after SM exposure led to significant improvements in key physiologic measures, including oxygenation, pH, and shunt fraction, as well as decreased neutrophil infiltration and protein leakage in the lung (Jugg et al, 2013).…”

Section: Targeting Reactive Oxygen and Nitrogen Speciesmentioning

confidence: 99%

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Mustard vesicant-induced lung injury: Advances in therapy

Weinberger

Malaviya

Sunil

et al. 2016

Toxicology and Applied Pharmacology

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Most mortality and morbidity following exposure to vesicants such as sulfur mustard is due to pulmonary toxicity. Acute injury is characterized by epithelial detachment and necrosis in the pharynx, trachea and bronchioles, while long-term consequences include fibrosis and in some instances, cancer. Current therapies to treat mustard poisoning are primarily palliative and do not target underlying pathophysiologic mechanisms. New knowledge about vesicant-induced pulmonary disease pathogenesis has led to the identification of potentially efficacious strategies to reduce injury by targeting inflammatory cells and mediators including reactive oxygen and nitrogen species, proteases and proinflammatory/cytotoxic cytokines. Therapeutics under investigation include corticosteroids, N-acetyl cysteine, which has both mucolytic and antioxidant properties, inducible nitric oxide synthase inhibitors, liposomes containing superoxide dismutase, catalase, and/or tocopherols, protease inhibitors, and cytokine antagonists such as anti-tumor necrosis factor (TNF)-α antibody and pentoxifylline. Antifibrotic and fibrinolytic treatments may also prove beneficial in ameliorating airway obstruction and lung remodeling. More speculative approaches include inhibitors of transient receptor potential channels, which regulate pulmonary epithelial cell membrane permeability, non-coding RNAs and mesenchymal stem cells. As mustards represent high priority chemical threat agents, identification of effective therapeutics for mitigating toxicity is highly significant.

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Section: Targeting Reactive Oxygen and Nitrogen Speciesmentioning

confidence: 99%

Section: Targeting Reactive Oxygen and Nitrogen Speciesmentioning

confidence: 99%

Mustard vesicant-induced lung injury: Advances in therapy

Weinberger

Malaviya

Sunil

et al. 2016

Toxicology and Applied Pharmacology

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“…This is thought to be due in part to activation of the transcription factor AP-1 and upregulation of cyclin-D1 (Mukhopadhyay et al, 2009; Rahman, 2000). TNFα-mediated proliferation is thought to contribute to epithelial thickening and pulmonary fibrosis (Allen and Spiteri, 2002; Sasaki et al, 2000).…”

Section: Biological Activities Of Tnfαmentioning

confidence: 99%

Anti-TNFα therapy in inflammatory lung diseases

Malaviya

Laskin

2017

Pharmacology & Therapeutics

190

137

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Increased levels of tumor necrosis factor (TNF) α have been linked to a number of pulmonary inflammatory diseases including asthma, chronic obstructive pulmonary disease (COPD), acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), sarcoidosis, and interstitial pulmonary fibrosis (IPF). TNFα plays multiple roles in disease pathology by inducing an accumulation of inflammatory cells, stimulating the generation of inflammatory mediators, and causing oxidative and nitrosative stress, airway hyperresponsiveness and tissue remodeling. TNF-targeting biologics, therefore, present a potentially highly efficacious treatment option. This review summarizes current knowledge on the role of TNFα in pulmonary disease pathologies, with a focus on the therapeutic potential of TNFα-targeting agents in treating inflammatory lung diseases.

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“…We decided to analyse these markers as they belong to three different marker groups that may be related to cancer and/or to inflammatory diseases. p27, Skp2, Cox2, CycD1 and Ki67 are considered as tumour and/or proliferation markers (Huang et al, 2003;Siggelkow et al, 2004;Adjei, 2005;Vig-Varga et al, 2006;Garg et al, 2008;Park et al, 2008;Chang et al, 2009;Meeran et al, 2009;Mukhopadhyay et al, 2009), ImAnOx and carbonyls are oxidative markers (Nyström, 2005;Bahar et al, 2007) and MMP-9, -3 and -2 are MMPs that are expressed in various pathological processes such as inflammation and cancer and also in response to infections (Korpos et al, 2009;Oikonomidi et al, 2009;Vanlaere and Libert, 2009). Enhanced oxidative stress characterises both inflammation and cancer; all other markers analysed were also shown previously to be associated with inflammation, as well as with oxidative stress, presumably mediated through the activation of NF-kB (Huang et al, 2003;Vig-Varga et al, 2006;Park et al, 2008;Gonda et al, 2009;Karalis et al, 2009;Ku et al, 2009;Perricone et al, 2009;Víctor et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Pleural fluid analysis of lung cancer vs benign inflammatory disease patients

et al. 2010

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BACKGROUND: Correct diagnosis of pleural effusion (PE) as either benign or malignant is crucial, although conventional cytological evaluation is of limited diagnostic accuracy, with relatively low sensitivity rates. METHODS: We identified biological markers accurately detected in a simple PE examination. We analysed data from 19 patients diagnosed with lung cancer (nine adeno-Ca, five non-small-cell Ca (not specified), four squamous-cell Ca, one large-cell Ca) and 22 patients with benign inflammatory pathologies: secondary to trauma, pneumonia or TB. RESULTS: Pleural effusion concentrations of seven analysed biological markers were significantly lower in lung cancer patients than in benign inflammatory patients, especially in matrix metalloproteinase (MMP)-9, MMP-3 and CycD1 (lower by 65% (Po0.000003), 40% (Po0.0007) and 34% (Po0.0001), respectively), and in Ki67, ImAnOx, carbonyls and p27. High rates of sensitivity and specificity values were found for MMP-9, MMP-3 and CycD1: 80 and 100%; 87 and 73%; and 87 and 82%, respectively. CONCLUSIONS: Although our results are of significant merit in both the clinical and pathogenetic aspects of lung cancer, further research aimed at defining the best combination for marker analysis is warranted. The relative simplicity in analysing these markers in any routine hospital laboratory may result in its acceptance as a new diagnostic tool.

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Role of MAPK/AP-1 signaling pathway in the protection of CEES-induced lung injury by antioxidant liposome

Cited by 40 publications

References 33 publications

Mustard vesicant-induced lung injury: Advances in therapy

Mustard vesicant-induced lung injury: Advances in therapy

Anti-TNFα therapy in inflammatory lung diseases

Pleural fluid analysis of lung cancer vs benign inflammatory disease patients

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