Upregulation of Gelatinases and Epithelial–Mesenchymal Transition in Small Airway Remodeling Associated with Chronic Exposure to Wood Smoke

Zou, Yimin; Li, Shaoxing; Zou, Weifeng; Hu, Guoping; Zhou, Yumin; Peng, Gongyong; He, Fang; Li, Bing; Ran, Pixin

doi:10.1371/journal.pone.0096708

Cited by 22 publications

(19 citation statements)

References 34 publications

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“…82 Peribronchiolar fibrosis was also seen in the lungs of exposed rats to biomass and cigarette smoke, as evident by increased number of fibroblasts around the small airways accompanied by type I collagen deposition in the airway walls. 38 These findings in rodents are similar to the limited studies done in humans that demonstrate increased expression of MMP-9 and MMP-12 in the sputum samples of exposed women exposed to open fire stoves. 83 However, exposure of rats for 3 months to wood smoke concentrations that resemble those found in developing countries (10 mg/m 3 ) did not change rodent pulmonary function.…”

Section: Chronic Exposuresupporting

confidence: 83%

“…34,35,37 Pathologic Data In a rat model, similar emphysematous changes were seen in the lungs of animals exposed to wood smoke as those exposed to tobacco smoke. 38 In humans, a similar type of emphysema was seen in autopsies of women with COPD due to biomass smoke exposure and those with COPD due to tobacco smoking (mainly centrilobular emphysema), but more severe emphysema was reported in the tobacco smokers than biomass smoke-exposed women on macroscopic pathologic examination. 35…”

Section: Severitymentioning

confidence: 85%

“…Chronic exposure to wood smoke in guinea pigs leads to marked upregulation and production of matrix metalloproteinases (MMP-9, MMP-12) and tissue inhibitors of MMPs in the airway epithelial cells. 38,81 Those proteins are believed to play a role in the development of emphysema. 82 Peribronchiolar fibrosis was also seen in the lungs of exposed rats to biomass and cigarette smoke, as evident by increased number of fibroblasts around the small airways accompanied by type I collagen deposition in the airway walls.…”

Section: Chronic Exposurementioning

confidence: 99%

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Chronic Obstructive Pulmonary Disease Secondary to Household Air Pollution

Assad

Balmes

Mehta³

et al. 2015

Semin Respir Crit Care Med

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Approximately 3 billion people around the world cook and heat their homes using solid fuels in open fires and rudimentary stoves, resulting in household air pollution. Household air pollution secondary to indoor combustion of solid fuel is associated with multiple chronic obstructive pulmonary disease (COPD) outcomes. The exposure is associated with both chronic bronchitis and emphysema phenotypes of COPD as well as a distinct form of obstructive airway disease called bronchial anthracofibrosis. COPD from household air pollution differs from COPD from tobacco smoke with respect to its disproportionately greater bronchial involvement, lesser emphysematous change, greater impact on quality of life, and possibly greater oxygen desaturation and pulmonary hypertensive changes. Interventions that decrease exposure to biomass smoke may decrease the risk for incident COPD and attenuate the longitudinal decline in lung function, but more data on exposure-response relationships from well-designed longitudinal studies are needed.

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Section: Chronic Exposuresupporting

confidence: 83%

Section: Severitymentioning

confidence: 85%

Section: Chronic Exposurementioning

confidence: 99%

See 1 more Smart Citation

Chronic Obstructive Pulmonary Disease Secondary to Household Air Pollution

Assad

Balmes

Mehta³

et al. 2015

Semin Respir Crit Care Med

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“…It should be noted that these exposures were intended to simulate indoor exposure of villagers in Xuan County, China, and the coal used for this domestic purpose differs substantially from coal used for electricity generation. More recently, Zou et al (2014) assessed small-airway remodeling in rats exposed to wood smoke for 4 to 7 months in an effort to increase mechanistic understanding of chronic obstructive pulmonary disease (COPD) associated with chronic wood smoke exposure. Lung tissues were examined with morphometric measurements, immunohistochemistry, and Western blotting.…”

Section: Toxicological Studiesmentioning

confidence: 99%

Long-term particulate matter exposure: Attributing health effects to individual PM components

Wyzga

Rohr

2015

Journal of the Air & Waste Management Association

117

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While most in the scientific community are of the opinion that the composition of fine particulate matter (PM 2.5 ) is an important driver of resultant health effects, there is still some degree of uncertainty regarding those components considered to be most harmful. Reviews of the subject from several perspectives have been published, but to our knowledge a comprehensive review of the epidemiological and toxicological literature related to long-term exposure to PM 2.5 components does not exist. We reviewed published epidemiological studies that were of a cohort design, included at least one PM component as well as PM 2.5 mass, and included quantitative analysis to relate health outcomes to individual components. Toxicological studies were included if they were ≥5 months in duration and either included at least one PM component as well as PM mass or focused on a specific PM or emissions type. Overall, we find that epidemiological and toxicological evidence for long-term effects of PM components is limited, in contrast to the short-term literature, which is more plentiful. Epidemiological literature suggests that a number of components are associated with health effects, and that no component is unequivocally not so associated. Toxicological studies that can more easily identify potentially causal components are generally limited to long-term studies using concentrated ambient particles (CAPs), of which few long-term studies exist. Epidemiological study designs that utilize existing monitoring data routinely collected by the U.S. Environmental Protection Agency would be valuable additions to the literature, as would novel toxicological studies that incorporate innovative designs to separate components or groups of components, such as denuders, filtration, or other approaches. From a policy perspective, it is important to more comprehensively investigate this issue so that if particular constituents are determined to be more potent in inducing health effects, their sources can be controlled.Implications: Understanding the components of PM 2.5 that are most harmful to human health is a critical policy issue. This review examined the epidemiological and toxicological literature related to long-term exposure to PM components and found that, unlike the literature on short-term health effects, there is insufficient information to make clear inferences about causal components. There is a need for further research in this area to exploit existing PM monitoring data in epidemiological studies and to design experimental studies that are able to tease out the effects of multiple constituents.

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“…The paraffin-embedded slides were dewaxed, hydrated, and the antigen retrieved with the sodium citrate method for 5 minutes at high pressure [15]. The slices were incubated in 3% hydrogen peroxide for 30 minutes and then were blocked for 30 minutes.…”

Section: Immunohistochemistry (Ihc) and Mean Optical Density Analysismentioning

confidence: 99%

Suppression of Rcn3 in the alveolar epithelial cells may have beneficial effect against COPD

Zhang

Wang

Jin

et al. 2020

Preprint

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Background: Chronic obstructive pulmonary disease (COPD) is a highly prevalent lung disease worldwide and imposes increasing disease burdens globally. COPD is characterized by irreversible airflow obstruction. Emphysema is one of the primary pathological features causing the irreversible decline of pulmonary function, while the precise mechanisms behind emphysema remain unclear. Reticulocalbin 3 (Rcn3) is an endoplasmic reticulum (ER) lumen protein localized in the secretory pathway of living cells. We have reported that Rcn3 in type II alveolar epithelial cell (AECIIs) plays a critical role in perinatal lung development and bleomycin-induced lung injury-repair. Since is associated with alveolar epithelial disruption, Rcn3 might be involved in the development of emphysema during COPD. Materials and Methods : We examined Rcn3 expression in lung specimens from patients (44 COPD patients and 26 non-COPD control patients) undergoing lung lobectomy or pneumonectomy. Mouse models of COPD and emphysema were established by cigarette smoke (CS) exposure and intratracheal installation of pancreatic porcine elastase (PPE), respectively. Rcn3 expression was detected in the lung tissues from these mice. Furthermore, conditional knockout (CKO) mice with Rcn3 deletion specific to AECIIs, were used to explore the role of Rcn3 in PPE-induced emphysema progression. Rcn3 protein expression in lung tissues were evaluated by Western blot and immunohistochemistry. Rcn3 mRNA expression in lung tissues was detected by qPCR.Results : Compared with non-COPD patients, Rcn3 expression was significantly increased in the lung specimens from COPD patients. Rcn3 expression was also significantly up-regulated in the lung tissues from COPD mice and emphysematous mice. Moreover, selective ablation of Rcn3 in AEC IIs significantly alleviated severity of the mouse emphysema in response to intratracheal installation of PPE.Conclusions: Our data, for the first time, indicated that Rcn3 in AECIIs might play a role in modulating the progression of emphysema, and thus be involved in the development of COPD. Suppression of Rcn3 expression in AECIIs may have a beneficial effect on COPD.This work was supported by National Natural Science Foundation of China (No. 81641004).

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Upregulation of Gelatinases and Epithelial–Mesenchymal Transition in Small Airway Remodeling Associated with Chronic Exposure to Wood Smoke

Cited by 22 publications

References 34 publications

Chronic Obstructive Pulmonary Disease Secondary to Household Air Pollution

Chronic Obstructive Pulmonary Disease Secondary to Household Air Pollution

Long-term particulate matter exposure: Attributing health effects to individual PM components

Suppression of Rcn3 in the alveolar epithelial cells may have beneficial effect against COPD

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