Oxidative stress, respiratory muscle dysfunction, and potential therapeutics in chronic obstructive pulmonary disease

Zuo, Li; Hallman, Allison H.; Yousif, Marvin K.; Chien, Michael T.

doi:10.1007/s11515-012-1251-x

Cited by 39 publications

(30 citation statements)

References 83 publications

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“…Particulate pollution is a serious environmental problem that is influencing air quality as well as regional and global climates, and epidemiological surveys show that air pollution may have negative effects on the human body, especially the respiratory system (Pope et al 2002; Balashazy et al 2003; Pope et al 2009; Shah et al 2013; Atkinson et al 2014; Beelen et al 2015). Additionally, numerous investigations on PM2.5 and human health were reported, mainly focusing on its cytotoxic effects (Laing et al 2010; Ma et al 2015; Deng et al 2014) and effect of reactive oxygen species (Ni et al 2015; Zuo et al 2012; Jiang et al 2014). The contributions of PM2.5, the main toxicological component of air pollution, to lung cancer are complex, and the specific mechanisms through which different genes regulate lung tumor growth and progression are not well defined.…”

Section: Discussionmentioning

confidence: 99%

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

et al. 2016

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BackgroundIncreasing urbanization and associated air pollution, including elevated levels of particulate matter (PM), are strongly correlated with the development of various respiratory diseases. In particular, PM2.5 has been implicated in promoting lung cancer initiation, growth and progression. Cell migration and proliferation are crucial for the progression of cancer. However, the molecular signatures and biological networks representing the distinct and shared features of non-small cell lung cancer (NSCLC) after PM2.5 exposure are unknown.ResultsFunctional assays demonstrated higher proliferation, migration and invasion of cancer cells stimulated with PM2.5. To investigate the complicated mechanisms, we performed global transcriptome profiling of the A549 cell line. Particularly, transcriptome sequencing revealed invasive characteristics reminiscent of cancer cells. By comparing the transcriptomes, we identified distinct molecular signatures and cellular processes defining the invasive and proliferative properties of PM2.5-exposed cells, respectively. Interestingly, under the PM2.5-stimulated condition, the A549 and H1299 cells strengthened obviously properties in motility and proliferation. Based on the network model reconstructing the shared protein–protein interactions, we selected the two most up-regulated genes, interleukin-1β (IL1β) and matrix metalloprotease 1 (MMP1), as key regulators responsible for the effects of PM2.5 exposure. Notably, IL1β and MMP1 expression was elevated in independent assays, which was further enhanced by PM2.5.ConclusionTaken together, our systems approach to investigating PM2.5 exposure provides a basis to identify key regulators responsible for the pathological features of NSCLC.

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Section: Discussionmentioning

confidence: 99%

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

et al. 2016

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“…Previous research has shown increased oxidative stress and escalated catalase activity during low-oxygen conditions, as well as in asthma and COPD subjects (136,145,147,149). This enhanced antioxidant enzymatic activity is an indirect result of oxidative stress induced by COPD (136).…”

Section: Role Of Reactive Oxygen Species In Copdmentioning

confidence: 91%

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Zuo

Sergakis

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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216

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Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

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“…For instance, exogenous antioxidant supplements have been shown to suppress muscle contractility while the addition of H 2 O 2 relieves such an effect, suggesting that oxidants (at low levels) may be imperative in facilitating muscle contraction (Reid et al, 1993; Powers and Jackson, 2008). However, the overproduction of ROS induced by exhaustive exercise training or other stresses, along with compromised antioxidant defenses, can lead to oxidative stress and related tissue damage (Powers et al, 2011b; Zuo et al, 2012). Interestingly, proper exercise (moderate to high intensity exercise) stimulates the adaptive responses and strengthens the endogenous antioxidant defense systems to combat excessive ROS thereby maintaining muscle redox balance (Parker et al, 2014; Zuo et al, 2015b).…”

Section: Introductionmentioning

confidence: 99%

Redox Mechanism of Reactive Oxygen Species in Exercise

et al. 2016

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It is well known that regular exercise can benefit health by enhancing antioxidant defenses in the body. However, unaccustomed and/or exhaustive exercise can generate excessive reactive oxygen species (ROS), leading to oxidative stress-related tissue damages and impaired muscle contractility. ROS are produced in both aerobic and anaerobic exercise. Mitochondria, NADPH oxidases and xanthine oxidases have all been identified as potential contributors to ROS production, yet the exact redox mechanisms underlying exercise-induced oxidative stress remain elusive. Interestingly, moderate exposure to ROS is necessary to induce body's adaptive responses such as the activation of antioxidant defense mechanisms. Dietary antioxidant manipulation can also reduce ROS levels and muscle fatigue, as well as enhance exercise recovery. To elucidate the complex role of ROS in exercise, this review updates on new findings of ROS origins within skeletal muscles associated with various types of exercises such as endurance, sprint and mountain climbing. In addition, we will examine the corresponding antioxidant defense systems as well as dietary manipulation against damages caused by ROS.

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Oxidative stress, respiratory muscle dysfunction, and potential therapeutics in chronic obstructive pulmonary disease

Cited by 39 publications

References 83 publications

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

The effects for PM2.5 exposure on non-small-cell lung cancer induced motility and proliferation

Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Redox Mechanism of Reactive Oxygen Species in Exercise

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