Mass Resolution and Mass Accuracy: How Much Is Enough?

Marshall, Alan G.; Blakney, Greg T.; Chen, Tong; Kaiser, Nathan K.; McKenna, Amy M.; Rodgers, Ryan P.; Ruddy, Brian M.; Xian, Feng

doi:10.5702/massspectrometry.s0009

Cited by 49 publications

(53 citation statements)

References 30 publications

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“…In Ctsc −/− mice IL-33 processing did not occur during the peak of ALT-driven immune cell infiltration into the lung but instead correlated with ALT-driven damage to the airway epithelium. We discovered that IL-33 released from damaged airway epithelial cells was processed by calpains, necrosis-activated Ca 2+ -dependent proteases 38 – 40 , that were previously shown to cleave recombinant IL-33 in a transfected cell system 18 . In addition, we have demonstrated for the first time that processing of IL-33 by calpain-1 occurred within its activation domain 14 to enhance its biological potency.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 is activated by allergen- and necrosis-associated proteolytic activities to regulate its alarmin activity during epithelial damage

Scott¹,

Majithiya²,

Sandén

et al. 2018

Sci Rep

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Interleukin (IL)-33 is an IL-1 family alarmin released from damaged epithelial and endothelial barriers to elicit immune responses and allergic inflammation via its receptor ST2. Serine proteases released from neutrophils, mast cells and cytotoxic lymphocytes have been proposed to process the N-terminus of IL-33 to enhance its activity. Here we report that processing of full length IL-33 can occur in mice deficient in these immune cell protease activities. We sought alternative mechanisms for the proteolytic activation of IL-33 and discovered that exogenous allergen proteases and endogenous calpains, from damaged airway epithelial cells, can process full length IL-33 and increase its alarmin activity up to ~60-fold. Processed forms of IL-33 of apparent molecular weights ~18, 20, 22 and 23 kDa, were detected in human lungs consistent with some, but not all, proposed processing sites. Furthermore, allergen proteases degraded processed forms of IL-33 after cysteine residue oxidation. We suggest that IL-33 can sense the proteolytic and oxidative microenvironment during tissue injury that facilitate its rapid activation and inactivation to regulate the duration of its alarmin function.

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Section: Discussionmentioning

confidence: 99%

Interleukin-33 is activated by allergen- and necrosis-associated proteolytic activities to regulate its alarmin activity during epithelial damage

Scott¹,

Majithiya²,

Sandén

et al. 2018

Sci Rep

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“…Then, molecular formulas with assignment errors >0.3 ppm and those from the blank filter extract were excluded from further processing. In general, the criterion of the mass accuracy with less than 0.5‐ppm errors has been accepted for the data sets derived from ultrahigh‐resolution MS analysis (Choi, Ryu , et al, ; Marshall et al, ). A van Krevelen plot was used to visualize the assigned chemical compositions based on the atomic hydrogen‐to‐carbon and oxygen‐to‐carbon ratios (as shown in Figure ; Kim et al, ).…”

Section: Methodsmentioning

confidence: 99%

Influence of Biogenic Organics on the Chemical Composition of Arctic Aerosols

Choi

Jang

Yoon

et al. 2019

Global Biogeochemical Cycles

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We use an ultrahigh‐resolution 15‐T Fourier transform ion cyclotron resonance mass spectrometer to elucidate the compositional changes in Arctic organic aerosols collected at Ny‐Ålesund, Svalbard, in May 2015. The Fourier transform ion cyclotron resonance mass spectrometer analysis of airborne organic matter provided information on the molecular compositions of aerosol particles collected during the Arctic spring period. The air mass transport history, combined with satellite‐derived geographical information and chlorophyll concentration data, revealed that the molecular compositions of organic aerosols drastically differed depending on the origin of the potential source region. The protein and lignin compound populations contributed more than 70% of the total intensity of assigned molecules when the air masses mainly passed over the ocean region. Interestingly, the intensity of microbe‐derived organics (protein and carbohydrate compounds) was positively correlated with the air mass exposure to phytoplankton biomass proxied as chlorophyll. Furthermore, the intensities of lignin and unsaturated hydrocarbon compounds, typically derived from terrestrial vegetation, increased with an increase in the advection time of the air mass over the ocean domain. These results suggest that the accumulation of dissolved biogenic organics in the Arctic Ocean possibly derived from both phytoplankton and terrestrial vegetation could significantly influence the chemical properties of Arctic organic aerosols during a productive spring period. The interpretation of molecular changes in organic aerosols using an ultrahigh‐resolution mass spectrometer could provide deep insight for understanding organic aerosols in the atmosphere over the Arctic and the relationship of organic aerosols with biogeochemical processes in terms of aerosol formation and environmental changes.

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“…1H right). Although the epicardial-restricted Gata5 Cre and Wt1 GFP/Cre mice displayed ectopic Cre expression in the endocardial/endothelial and myocardial cells of the developing heart 15 , our data demonstrate that both G5-Cre and Wt1-CreGFP efficiently removes PKR1 from the epicardium without significantly altering myocardial or endothelial PKR1 expression.…”

Section: Resultsmentioning

confidence: 64%

Prokineticin receptor-1 signaling promotes Epicardial to Mesenchymal Transition during heart development

Arora

Boulberdaa

Qureshi

et al. 2016

Sci Rep

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The epicardium plays an essential role in coronary artery formation and myocardial development. However, signals controlling the developing epicardium and epicardial-mesenchymal transition (EMT) in the normal and diseased adult heart are studied less rigorously. Here we investigated the role of angiogenic hormone, prokineticin-2 and its receptor PKR1 in the epicardium of developing and adult heart. Genetic ablation of PKR1 in epicardium leads to partial embryonic and postnatal lethality with abnormal heart development. Cardiac developmental defects are manifested in the adult stage as ischemic cardiomyopathy with systolic dysfunction. We discovered that PKR1 regulates epicardial-mesenchymal transition (EMT) for epicardial-derived progenitor cell (EPDC), formation. This event affects at least three consequential steps during heart development: (i) EPDC and cardiomyocyte proliferation involved in thickening of an outer compact ventricular chamber wall, (ii) rhythmicity, (iii) formation of coronary circulation. In isolated embryonic EPDCs, overexpression or activation of PKR1 alters cell morphology and EMT markers via activating Akt signaling. Lack of PKR1 signal in epicardium leads to defective heart development and underlies the origin of congenital heart disease in adult mice. Our mice provide genetic models for congenital dysfunction of the heart and should facilitate studies of both pathogenesis and therapy of cardiac disorders in humans.

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Mass Resolution and Mass Accuracy: How Much Is Enough?

Cited by 49 publications

References 30 publications

Interleukin-33 is activated by allergen- and necrosis-associated proteolytic activities to regulate its alarmin activity during epithelial damage

Interleukin-33 is activated by allergen- and necrosis-associated proteolytic activities to regulate its alarmin activity during epithelial damage

Influence of Biogenic Organics on the Chemical Composition of Arctic Aerosols

Prokineticin receptor-1 signaling promotes Epicardial to Mesenchymal Transition during heart development

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