Receptor for advanced glycation end-products and environmental exposure related obstructive airways disease: a systematic review

Haider, Syed Hissam; Oskuei, Assad; Crowley, George; Kwon, Sophia; Lam, Rachel; Riggs, Jessica; Mikhail, Maryann; Talusan, Angela; Veerappan, Arul; Kim, James S.; Caraher, Erin J.; Nolan, Anna

doi:10.1183/16000617.0096-2018

Cited by 20 publications

(19 citation statements)

References 89 publications

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“…RAGE is abundantly expressed in the lung, at baseline predominantly in alveolar type I cells toward the basal membrane, but it can be activated in many other cell types upon exposure to RAGE ligands (304). Numerous studies have established associations of RAGE and its soluble decoy receptor sRAGE with lung injury and disease (303,304,306,307). RAGE-mediated downstream signalling depends on the identity and oligomerization state of the ligand and the tissue context.…”

Section: Effects Mediated Through the Receptor For Advanced Glycation Endproductsmentioning

confidence: 99%

Collagen Biosynthesis, Processing, and Maturation in Lung Ageing

et al. 2021

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In addition to providing a macromolecular scaffold, the extracellular matrix (ECM) is a critical regulator of cell function by virtue of specific physical, biochemical, and mechanical properties. Collagen is the main ECM component and hence plays an essential role in the pathogenesis and progression of chronic lung disease. It is well-established that many chronic lung diseases, e.g., chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) primarily manifest in the elderly, suggesting increased susceptibility of the aged lung or accumulated alterations in lung structure over time that favour disease. Here, we review the main steps of collagen biosynthesis, processing, and turnover and summarise what is currently known about alterations upon lung ageing, including changes in collagen composition, modification, and crosslinking. Recent proteomic data on mouse lung ageing indicates that, while the ER-resident machinery of collagen biosynthesis, modification and triple helix formation appears largely unchanged, there are specific changes in levels of type IV and type VI as well as the two fibril-associated collagens with interrupted triple helices (FACIT), namely type XIV and type XVI collagens. In addition, levels of the extracellular collagen crosslinking enzyme lysyl oxidase are decreased, indicating less enzymatically mediated collagen crosslinking upon ageing. The latter contrasts with the ageing-associated increase in collagen crosslinking by advanced glycation endproducts (AGEs), a result of spontaneous reactions of protein amino groups with reactive carbonyls, e.g., from monosaccharides or reactive dicarbonyls like methylglyoxal. Given the slow turnover of extracellular collagen such modifications accumulate even more in ageing tissues. In summary, the collective evidence points mainly toward age-induced alterations in collagen composition and drastic changes in the molecular nature of collagen crosslinks. Future work addressing the consequences of these changes may provide important clues for prevention of lung disease and for lung bioengineering and ultimately pave the way to novel targeted approaches in lung regenerative medicine.

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Section: Effects Mediated Through the Receptor For Advanced Glycation Endproductsmentioning

confidence: 99%

Collagen Biosynthesis, Processing, and Maturation in Lung Ageing

et al. 2021

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“…Currently, there is significant interest in the role of the receptor for advanced glycation end products (RAGE) in COPD pathogenesis as it is both a genetic determinant of low lung function and COPD susceptibility. It is also involved in the cellular and molecular response to cigarette smoke (CS) exposure 1‐4 …”

Section: Introductionmentioning

confidence: 99%

RAGE and TLR4 differentially regulate airway hyperresponsiveness: Implications for COPD

Allam

Faiz

Lam

et al. 2020

Allergy

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Background The receptor for advanced glycation end products (RAGE) and Toll‐like receptor 4 (TLR4) is implicated in COPD. Although these receptors share common ligands and signalling pathways, it is not known whether they act in concert to drive pathological processes in COPD. We examined the impact of RAGE and/or TLR4 gene deficiency in a mouse model of COPD and also determined whether expression of these receptors correlates with airway neutrophilia and airway hyperresponsiveness (AHR) in COPD patients. Methods We measured airway inflammation and AHR in wild‐type, RAGE−/−, TLR4−/− and TLR4−/−RAGE−/− mice following acute exposure to cigarette smoke (CS). We also examined the impact of smoking status on AGER (encodes RAGE) and TLR4 bronchial gene expression in patients with and without COPD. Finally, we determined whether expression of these receptors correlates with airway neutrophilia and AHR in COPD patients. Results RAGE−/− mice were protected against CS‐induced neutrophilia and AHR. In contrast, TLR4−/− mice were not protected against CS‐induced neutrophilia and had more severe CS‐induced AHR. TLR4−/−RAGE−/− mice were not protected against CS‐induced neutrophilia but were partially protected against CS‐induced mediator release and AHR. Current smoking was associated with significantly lower AGER and TLR4 expression irrespective of COPD status, possibly reflecting negative feedback regulation. However, consistent with preclinical findings, AGER expression correlated with higher sputum neutrophil counts and more severe AHR in COPD patients. TLR4 expression did not correlate with neutrophilic inflammation or AHR. Conclusions Inhibition of RAGE but not TLR4 signalling may protect against airway neutrophilia and AHR in COPD.

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“…Cases of WTC-OAD had either WTC-Lung Injury (WTC-LI; FEV 1 <LLN) and/or Airway Hyperresponsiveness (AHR;positive methacholine or positive bronchodilator testing) at any time point post-9/11 (N=921). (22)(23)(24)(25)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62)(63)(64)(65)(66)(67) Cases of WTC-OAD were compared to N=3,094 without WTC-OAD at any time after 9/11.…”

Section: Methodsmentioning

confidence: 99%

Dietary Phenotype and Advanced Glycation End-Products Predict WTC-Obstructive Airways Disease: a Longitudinal Observational Study

Lam

Kwon

Riggs

et al. 2020

Preprint

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BACKGROUND. Diet is a modifier of metabolic syndrome which in turn is associated with World Trade Center Obstructive Airways Disease(WTC-OAD). We have designed this study to 1.assess the dietary phenotype(food types, physical activity, and dietary habits) of the Fire Department of New York(FDNY) WTC-Health Program(WTC-HP) cohort and 2.quantify the association of dietary quality and its advanced glycation end product(AGE) content with the development of WTC-OAD.METHODS. WTC-OAD, defined as developing WTC-Lung Injury(WTC-LI;FEV1<LLN) and/or airway hyperreactivity(AHR;positive methacholine and/or positive bronchodilator response). Rapid Eating and Activity Assessment for Participants-Short Version(REAP-S) deployed on 3/1/2018 in the WTC-HP annual monitoring assessment. Clinical and REAP-S data of consented subjects was extracted(7/17/2019). Diet quality[low-(15-19), moderate-(20-29), and high-(30-39)] and AGE content per REAP-S questionnaire were assessed for association with WTC-OAD. Regression models adjusted for smoking,hyperglycemia,hypertension,age on 9/11,WTC-exposure,BMI and job description. RESULTS. N=9,508 completed the annual questionnaire, while N=4,015 completed REAP-S and had spirometry. WTC-OAD developed in N=921, while N=3,094 never developed WTC-OAD. Low- and moderate-dietary quality, eating more (processed meats,fried foods,sugary drinks), fewer(vegetables,whole-grains),and having a diet abundant in AGEs were significantly associated with WTC-OAD. Smoking was not a significant risk factor of WTC-OAD. CONCLUSIONS. REAP-S was successfully implemented in the FDNY WTC-HP monitoring questionnaire and produced valuable dietary phenotyping. Our observational study has identified low dietary quality and AGE abundant dietary habits as risk factors for pulmonary disease in the context of WTC-exposure. Dietary phenotyping, not only focuses our metabolomic/biomarker profiling but also further informs future dietary interventions that may positively impact particulate matter associated lung disease.

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Receptor for advanced glycation end-products and environmental exposure related obstructive airways disease: a systematic review

Cited by 20 publications

References 89 publications

Collagen Biosynthesis, Processing, and Maturation in Lung Ageing

Collagen Biosynthesis, Processing, and Maturation in Lung Ageing

RAGE and TLR4 differentially regulate airway hyperresponsiveness: Implications for COPD

Dietary Phenotype and Advanced Glycation End-Products Predict WTC-Obstructive Airways Disease: a Longitudinal Observational Study

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