Protein oxidation and degradation caused by particulate matter

Lai, Ching‐Huang; Lee, Chun-Nin; Bai, Kuan‐Jen; Yang, Yiyuan; Chuang, Kai Jen; Wu, Sheng‐Ming; Chuang, Hsiao-Chi

doi:10.1038/srep33727

Cited by 36 publications

(13 citation statements)

References 50 publications

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“…Soluble CD14, as determined in the present study, enhances lipopolysaccharide-induced activation of cells with low CD14 expression. Consistently, alterations in CD14 were previously reported to be associated with air pollution exposure [24,25]. However, we observed no association between air pollution and CD14.…”

Section: Discussionsupporting

confidence: 90%

Alterations by Air Pollution in Inflammation and Metals in Pleural Effusion of Pneumonia Patients

Bai

Chuang

Chen

et al. 2019

IJERPH

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Air pollution is known to increase the risk of pneumonia. However, the effects of air pollution on the pleural effusion of patients with pneumonia are unclear. The objective of this study was to investigate alterations in inflammatory–immune biomarkers by air pollution in patients with pneumonia by analyzing their pleural effusion. Patients who had undergone thoracentesis to drain their pleural effusion in a hospital were recruited for this study. Patients with pneumonia and those with congestive heart failure respectively served as the case and control groups. We observed that an increase of 1 ppb in one-year NO2 was associated with a decrease of 0.105 ng/mL in cluster of differentiation 62 (CD62) (95% confidence interval (CI) = −0.085, −0.004, p < 0.05) in the pleural effusion. Furthermore, we observed that an increase in one−year 1 ppb of NO2 was associated with a decrease of 0.026 ng/mL in molybdenum (Mo) (95% CI = −0.138, −0.020, p < 0.05). An increase in one-year 1 ppb of SO2 was associated with a decrease of 0.531 ng/mL in zinc (95% CI = −0.164, −0.006, p < 0.05). Also, an increase in one-year 1 ppb of O3 was associated with a decrease of 0.025 ng/mL in Mo (95% CI = −0.372, −0.053, p < 0.05). In conclusion, air pollution exposure, especially gaseous pollution, may be associated with the regulation of immune responses and changes in metal levels in the pleural effusion of pneumonia patients.

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Section: Discussionsupporting

confidence: 90%

Alterations by Air Pollution in Inflammation and Metals in Pleural Effusion of Pneumonia Patients

Bai

Chuang

Chen

et al. 2019

IJERPH

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“…The lack of protein turnover by the 20S Proteasome, is also evident by the accumulation of protein carbonyls, a marker of protein oxidation [90]. We found significant accumulation of protein carbonyls in 21 month nPM treated tissue, which mirrors similar in vitro particulate exposure [91]. The dichotomy between the age-associated rise in Proteasome levels, but the lack of a concurrent rise in subunit-specific activity, builds upon our findings in the nematode worm [45] and fruit-fly [92].…”

Section: Discussionmentioning

confidence: 57%

Aging attenuates redox adaptive homeostasis and proteostasis in female mice exposed to traffic-derived nanoparticles (‘vehicular smog’)

Pomatto

Cline

Woodward

et al. 2018

Free Radical Biology and Medicine

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Environmental toxicants are catalysts for protein damage, aggregation, and the aging process. Fortunately, evolution selected adaptive homeostasis as a system to mitigate such damage by expanding the normal capacity to cope with toxic stresses. Little is known about the subcellular degradative responses to proteins oxidatively damaged by air pollution. To better understand the impact of environmental toxicants upon the adaptive homeostatic response, female C57BL/6 mice were exposed for 10 weeks to filtered air or reaerosolized vehicular-derived nano-scale particulate matter (nPM), at which point tissues from young (6 month) and middle-aged (21 month) mice were studied. We found significant increases of proteolytic capacity in lung, liver, and heart. Up to two-fold increases were seen in the 20S Proteasome, the Immunoproteasome, the mitochondrial Lon protease, and NF-E2-related factor 2 (Nrf2), a major transcriptional factor for these and other stress-responsive genes. The responses were equivalent in all organs, despite the indirect input of inhaled particles to heart and liver which are downstream of lung. To our knowledge, this is the first exploration of proteostatic responses to oxidative damage by air pollution. Although, middle-aged mice had higher basal levels, their Nrf2-responsive-genes exhibited no response to nanoparticulate exposure. We also found a parallel age-associated rise in the Nrf2 transcriptional inhibitors, Bach1 and c-Myc which appear to attenuate adaptive responses in older mammals, possibly explaining the 'age-ceiling effect.' This report extends prior findings in male mice by demonstrating the involvement of proteolytic responses to traffic-related air pollution in lung, liver, and heart of female mice, with an age-dependent loss of adaptive homeostasis.

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“…Methionine oxidation also occurs with environmental stress, for example diesel exhaust particles. A recent study demonstrated that diesel exhaust particles activate MsrA-driven protein repair and activate autophagy and proteasomal protein degradation [54] . Our study contributes to the understanding of Msr biology under baseline conditions [55] when oxidative stress is not excessive by dissecting how the loss of reduction of methionine sulfoxide affects protein repair mechanisms and intersects with antioxidant signaling.…”

Section: Discussionmentioning

confidence: 99%

Defective protein repair under methionine sulfoxide A deletion drives autophagy and ARE-dependent gene transcription

et al. 2018

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ObjectiveReduction of oxidized methionines is emerging as a major protein repair pathway. The lack of methionine sulfoxide reductase A (MsrA) exacerbates cardiovascular disease phenotypes driven by increased oxidative stress. However, the role of MsrA on maintaining cellular homeostasis in the absence of excessive oxidative stress is less well understood.Methods and resultsConstitutive genetic deletion of MsrA increased formation of p62-containing protein aggregates, activated autophagy, and decreased a marker of apoptosis in vascular smooth muscle cells (VSMC). The association of Keap1 with p62 was augmented in MsrA-/- VSMC. Keap1 targets the transcription factor Nrf2, which regulates antioxidant genes, for proteasomal degradation. However, in MsrA-/- VSMC, the association of Nrf2 with Keap1 was diminished. Whereas Nrf2 mRNA levels were not decreased in MsrA-/- VSMC, we detected decreased ubiquitination of Nrf2 and a corresponding increase in total Nrf2 protein in the absence of biochemical markers of oxidative stress. Moreover, nuclear-localized Nrf2 was increased under MsrA deficiency, resulting in upregulation of Nrf2-dependent transcriptional activity. Consequently, transcription, protein levels and enzymatic activity of glutamate-cysteine ligase and glutathione reductase were greatly augmented in MsrA-/- VSMC.SummaryOur findings demonstrate that reversal of methionine oxidation is required for maintenance of cellular homeostasis in the absence of increased oxidative stress. These data provide the first link between autophagy and activation of Nrf2 in the setting of MsrA deletion.

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Protein oxidation and degradation caused by particulate matter

Cited by 36 publications

References 50 publications

Alterations by Air Pollution in Inflammation and Metals in Pleural Effusion of Pneumonia Patients

Alterations by Air Pollution in Inflammation and Metals in Pleural Effusion of Pneumonia Patients

Aging attenuates redox adaptive homeostasis and proteostasis in female mice exposed to traffic-derived nanoparticles (‘vehicular smog’)

Defective protein repair under methionine sulfoxide A deletion drives autophagy and ARE-dependent gene transcription

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