Estrogen deficiency promotes cigarette smoke–induced changes in the extracellular matrix in the lungs of aging female mice

Glassberg, Marilyn K.; Catanuto, Paola; Shahzeidi, Shahriar; Aliniazee, Muddassir; Lilo, Sarit; Rubio, Gustavo A.; Elliot, Sharon J.

doi:10.1016/j.trsl.2016.07.015

Cited by 10 publications

(7 citation statements)

References 63 publications

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“…A study in C57BL/6J mice showed that estrogen deficiency and an increased estrogen receptor α expression led to the development of emphysema in aging female mouse lungs, and that these conditions improved after 17β-estradiol (E2, 0.025 mg) treatment [ 31 , 32 ]. In a study in aging female C57BL/6J mice, the absence of E2 resulted in a decrease in hydroxyproline content, macrophage number, and respiratory chain complex-1 protein, particularly in estrogen-deficient mice exposed to cigarette smoke [ 33 ]. In addition, Tian et al reported that the effects of PM were stronger at high temperatures in elderly women, possibly due to menopause [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

The Impact of the Synergistic Effect of Temperature and Air Pollutants on Chronic Lung Diseases in Subtropical Taiwan

Chen

et al. 2021

JPM

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Previous studies have suggested an association between air pollution and lung disease. However, few studies have explored the relationship between chronic lung diseases classified by lung function and environmental parameters. This study aimed to comprehensively investigate the relationship between chronic lung diseases, air pollution, meteorological factors, and anthropometric indices. We conducted a cross-sectional study using the Taiwan Biobank and the Taiwan Air Quality Monitoring Database. A total of 2889 participants were included. We found a V/U-shaped relationship between temperature and air pollutants, with significant effects at both high and low temperatures. In addition, at lower temperatures (<24.6 °C), air pollutants including carbon monoxide (CO) (adjusted OR (aOR):1.78/Log 1 ppb, 95% CI 0.98–3.25; aOR:5.35/Log 1 ppb, 95% CI 2.88–9.94), nitrogen monoxide (NO) (aOR:1.05/ppm, 95% CI 1.01–1.09; aOR:1.11/ppm, 95% CI 1.07–1.15), nitrogen oxides (NOx) (aOR:1.02/ppm, 95% CI 1.00–1.05; aOR:1.06/ppm, 95% CI 1.04–1.08), and sulfur dioxide (SO2) (aOR:1.29/ppm, 95% CI 1.01–1.65; aOR:1.77/ppm, 95% CI 1.36–2.30) were associated with restrictive and mixed lung diseases, respectively. Exposure to CO, NO, NO2, NOx and SO2 significantly affected obstructive and mixed lung disease in southern Taiwan. In conclusion, temperature and air pollution should be considered together when evaluating the impact on chronic lung diseases.

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Section: Discussionmentioning

confidence: 99%

The Impact of the Synergistic Effect of Temperature and Air Pollutants on Chronic Lung Diseases in Subtropical Taiwan

Chen

et al. 2021

JPM

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“…Furthermore, this association with smoke and the discordant changes by exposure duration was present in the glycoprotein subset only and not in the collagen or proteoglycan subsets, although the composite list of all components did respond similarly (Table 9). Additionally, there is evidence of an effect of estrogen in ECM remodeling in mice exposed to chronic cigarette smoke [64]. This corresponds with the enrichment of estrogen biosynthesis genes within the exposure-response gene list (Table 7).…”

Section: Discussionmentioning

confidence: 74%

“…These genes are enriched in gene sets regulating biological processes such as the oxidative stress response through glutathione oxidation, metabolism pathways, xenobiotic responses, and the ECM biology (Table 8). ECM biology has long been associated with chronic smoke exposure [38, 47, 49, 63, 64]. However, a comparison of the response after acute smoke, and particularly after a single compared to five consecutive doses of cigarette smoke has not been previously assessed, to the best of our knowledge.…”

Section: Discussionmentioning

confidence: 99%

Dynamic changes in lung responses after single and repeated exposures to cigarette smoke in mice

et al. 2019

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Cigarette smoke is well recognized to cause injury to the airways and the alveolar walls over time. This injury usually requires many years of exposure, suggesting that the lungs may rapidly develop responses that initially protect it from this repetitive injury. Our studies tested the hypotheses that smoke induces an inflammatory response and changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the response of the lungs to smoke differs after 1 day compared to 5 days of exposure. Male and female wildtype (WT) and Scnn1b -transgenic (βENaC) mice, which have chronic bronchitis and emphysematous changes due to dehydrated mucus, were exposed to cigarette smoke or sham air conditions for 1 or 5 days. The inflammatory response and gene expression profiles were analyzed in lung tissue. Overall, the inflammatory response to cigarette smoke was mild, and changes in mediators were more numerous after 1 than 5 days. βENaC mice had more airspace leukocytes than WT mice, and smoke exposure resulted in additional significant alterations. Many genes and gene sets responded similarly at 1 and 5 days: genes involved in oxidative stress responses were upregulated while immune response genes were downregulated. However, certain genes and biological processes were regulated differently after 1 compared to 5 days. Extracellular matrix biology genes and gene sets were upregulated after 1 day but downregulated by 5 days of smoke compared to sham exposure. There was no difference in the transcriptional response to smoke between WT and βENaC mice or between male and female mice at either 1 or 5 days. Taken together, these studies suggest that the lungs rapidly alter gene expression after only one exposure to cigarette smoke, with few additional changes after four additional days of repeated exposure. These changes may contribute to preventing lung damage.

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“…Finally, oestrogen is an important regulator of toxic cigarette smoke metabolites through cytochrome P450 enzymes 1. In a mouse model of COPD, Glassberg et al reported that oestradiol administration after ovariectomy protected against cigarette smoke-induced alveolar septal destruction, macrophage infiltration and decreased other markers of inflammation compared with ovariectomy without oestradiol administration 40. In the same mouse model, however, non-ovariectomised female mice also had increased small airway remodelling following cigarette smoke exposure when compared with both male mice and ovariectomised female mice 41.…”

Section: Discussionmentioning

confidence: 99%

Female reproductive history in relation to chronic obstructive pulmonary disease and lung function in UK biobank: a prospective population-based cohort study

2019

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ObjectivesSex differences in respiratory physiology and predilection for developing chronic obstructive pulmonary disease (COPD) have been documented, suggesting that female sex hormones may influence pathogenesis. We investigated whether aspects of female reproductive health might play a role in risk of COPD among women.DesignPopulation-based prospective cohort study.SettingUK Biobank recruited across 22 centres in the UK between 2006 to 2010.Primary and secondary outcomes measuresWe examined a range of female reproductive health indicators in relation to risk of COPD-related hospitalisation/death (n=271 271) using Cox proportional hazards regression; and lung function (n=273 441) using linear regression.ResultsParity >3 was associated with greater risk of COPD-related hospitalisation/death (adjusted HR 1.45; 95% CI: 1.16 to 1.82) and lower forced expiratory volume at 1 second/forced vital capacity ratio (FEV1/FVC) (adjusted mean difference −0.06; 95% CI: -0.07 to 0.04). Any oral contraception use was associated with lower risk of COPD-related hospitalisation/death (adjusted HR 0.85; 95% CI: 0.74 to 0.97) and greater FEV1/FVC (adjusted mean difference 0.01; 95% CI: 0.003 to 0.03). Late menarche (age >15) and early menopause (age <47) were also associated with greater risk of COPD-related hospitalisation/death (but not lung function), while endometriosis was associated with greater FEV1/FVC (not COPD-related hospitalisation/death). Early menarche (age <12 years) was associated with lower FEV1/FVC (but not COPD hospitalisation/death). Associations with polycystic ovary syndrome (PCOS) or ovarian cysts, any hormone replacement therapy (HRT) use, hysterectomy-alone and both hysterectomy and bilateral oophorectomy were in opposing directions for COPD-related hospitalisation/death (greater risk) and FEV1/FVC (positive association).ConclusionsMultiple female reproductive health indicators across the life course are associated with COPD-related hospitalisation/death and lung function. Further studies are necessary to understand the opposing associations of PCOS/ovarian cysts, HRT and hysterectomy with COPD and objective measures of airway obstruction.

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Estrogen deficiency promotes cigarette smoke–induced changes in the extracellular matrix in the lungs of aging female mice

Cited by 10 publications

References 63 publications

The Impact of the Synergistic Effect of Temperature and Air Pollutants on Chronic Lung Diseases in Subtropical Taiwan

The Impact of the Synergistic Effect of Temperature and Air Pollutants on Chronic Lung Diseases in Subtropical Taiwan

Dynamic changes in lung responses after single and repeated exposures to cigarette smoke in mice

Female reproductive history in relation to chronic obstructive pulmonary disease and lung function in UK biobank: a prospective population-based cohort study

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