Ambient particulate matter exposure and cardiovascular diseases: a focus on progenitor and stem cells

Cui, Yuqi; Sun, Qinghua; Liu, Zhenguo

doi:10.1111/jcmm.12822

Cited by 36 publications

(21 citation statements)

References 156 publications

(201 reference statements)

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“…Current studies of effects of PM 2.5 exposure on BMSCs differentiation are limited, and mainly focus on endothelial progenitor cells (EPCs), which play a critical role in maintaining the structural and functional integrity of vasculature. It has been reported that PM 2.5–10 exposure significantly suppressed the number and function of stem cells (SCs) and EPCs in animals and humans [ 8 – 10 ]. Nevertheless, the mechanisms for the detrimental effects of PM on EPCs remain to be fully defined.…”

Section: Introductionmentioning

confidence: 99%

Crucial role of pro-inflammatory cytokines from respiratory tract upon PM2.5 exposure in causing the BMSCs differentiation in cells and animals

Jin

et al. 2017

Oncotarget

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Fine particulate matter exposure may cause health risk, including cardiovascular diseases and cancer. Bone marrow mesenchymal stem cell (BMSC), a typical model for evaluating pollutant toxicity, has been closely linked to these diseases, due to its characteristics of differentiation. We therefore studied the BMSCs differentiation and its roles in inflammatory activation in the respiratory tract upon PM2.5 exposure using both in vitro and in vivo models. BMSCs differentiation into endothelial-like cells (ELCs) and cancer-associated fibroblasts cells (CAFs) was enhanced in response to conditioned medium from PM2.5–treated 16HBE cells. PM2.5 elevated inflammatory cytokines’ expression and secretion in 16HBE cells. However, induction of differentiation markers was reduced when IL-1β, IL-6 and COX-2 neutralizing antibodies were added to the conditioned medium. Furthermore, PM2.5 induced ROS formation and NADPH oxidase (NOX) expression in 16HBE cells. DPI (inhibitor of ROS from NOX) or NAC (inhibitor of ROS) supplement reduced PM2.5-induced inflammatory activation and BMSCs differentiation. Likewise, a concomitant disorder of mitochondrial morphology and respiratory chain was observed. In addition, Rot or AA (inhibitor of mitochondrial complex I or III) supplement restored PM2.5-induced toxic effects. Moreover, the results coincided with the in vitro data obtained from SD rats post-exposed to different doses of PM2.5 for 30 days. PM2.5 enhanced the BMSCs differentiation and inflammatory cytokines’ expression in respiratory organs of SD rats, including lung and trachea tissue. This study uncovers that PM2.5 promotes the BMSCs differentiation via inflammatory activation mediated by ROS induction from NOX and mitochondria in the respiratory tract.

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Section: Introductionmentioning

confidence: 99%

Crucial role of pro-inflammatory cytokines from respiratory tract upon PM2.5 exposure in causing the BMSCs differentiation in cells and animals

Jin

et al. 2017

Oncotarget

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“…PM 2.5 can have negative effects on air quality and threatens human health. Furthermore, it can have effects on tissue-specific stem progenitor cells [2,3]. However, little is known about the mechanisms underlying the effects of PM 2.5 on stem progenitor cells, particularly hematopoietic stem progenitor cells (HSPCs).…”

Section: To the Editormentioning

confidence: 99%

Maternal exposure to fine particulate matter during pregnancy induces progressive senescence of hematopoietic stem cells under preferential impairment of the bone marrow microenvironment and aids development of myeloproliferative disease

et al. 2019

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“…17 – 20 In addition, air pollution is associated with inflammation around the bronchi, which may increase systemic inflammation and oxidative stress leading to obesity. 21 Animal experiments showed that air pollution can lead to weight gain and cardiorespiratory and metabolic dysfunction. 22 …”

Section: Introductionmentioning

confidence: 99%

<p>Impact of Commuting Mode on Obesity Among a Working Population in Beijing, China: Adjusting for Air Pollution</p>

Liu¹,

Tao²,

Zhang³

et al. 2020

DMSO

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Background Few studies have considered the interplay between commuting mode and air pollution on obesity. The aim of this study was to examine whether workplace air pollutants exposure modifying the associations between different commuting mode and obesity. Methods A cross-sectional study of workers in Beijing was conducted in 2016. The study sample comprised 10,524 participants aged 18 to 65 years old. Outcomes were defined as overall obesity (BMI≥ 28 kg/m 2 ) and abdominal obesity (WC ≥ 85 cm in men and WC ≥ 80 cm in women). Commuting modes were divided into walking, cycling, bus, subway, and car or taxi. Logistic regression models were used to estimate odds ratios relating commuting mode to overall and abdominal obesity and stratified by gender, controlling for covariates. Results The association between commuting mode and obesity was more strongly in men than women. In the fully adjusted models, compared with car or taxi commuters, cycling (men: OR=0.37, 95% CI=0.20 to 0.68) or bus (men: OR=0.58, 95% CI=0.36 to 0.94) counterparts had a lower risk of overall obesity. Compared with car or taxi commuters, walking (men: OR=0.57, 95% CI=0.36 to 0.91), bus (men: OR=0.59, 95% CI=0.39 to 0.89), or subway (men: OR=0.59, 95% CI=0.39 to 0.89) counterparts had a lower risk of abdominal obesity. We observed significant interactions between exposure PM 10 and cycling on overall obesity in men. After adjusting for air pollutants, the association between commuting mode and obesity was slightly strengthened. Conclusion This study findings indicate that active (walking or cycling) or public (bus or subway) commuting modes were protected factors for overall and abdominal obesity among men. Air pollutants do not obscure the benefits of active or public commuting for obesity. These associations support the policy for increasing active or public commuting as a strategy to reduce the prevalence of obesity.

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Ambient particulate matter exposure and cardiovascular diseases: a focus on progenitor and stem cells

Cited by 36 publications

References 156 publications

Crucial role of pro-inflammatory cytokines from respiratory tract upon PM2.5 exposure in causing the BMSCs differentiation in cells and animals

Crucial role of pro-inflammatory cytokines from respiratory tract upon PM2.5 exposure in causing the BMSCs differentiation in cells and animals

Maternal exposure to fine particulate matter during pregnancy induces progressive senescence of hematopoietic stem cells under preferential impairment of the bone marrow microenvironment and aids development of myeloproliferative disease

<p>Impact of Commuting Mode on Obesity Among a Working Population in Beijing, China: Adjusting for Air Pollution</p>

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