The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Circadian clock function is disrupted by environmental tobacco/cigarette smoke, leading to lung inflammation and injury via a SIRT1‐BMAL1 pathway
Open accessAbstract
Patients with obstructive lung diseases display abnormal circadian rhythms in lung function. We determined the mechanism whereby environmental tobacco/cigarette smoke (CS) modulates expression of the core clock gene BMAL1, through Sirtuin1 (SIRT1) deacetylase during lung inflammatory and injurious responses. Adult C57BL6/J and various mice mutant for SIRT1 and BMAL1 were exposed to both chronic (6 mo) and acute (3 and 10 d) CS, and we measured the rhythmic expression of clock genes, circadian rhythms of locomotor activity, lung function, and inflammatory and emphysematous responses in the lungs. CS exposure (100–300 mg/m 3 particulates) altered clock gene expression and reduced locomotor activity by disrupting the central and peripheral clocks and increased lung inflammation, causing emphysema in mice. BMAL1 was acetylated and degraded in the lungs of mice exposed to CS and in patients with chronic obstructive pulmonary disease (COPD), compared with lungs of the nonsmoking controls, linking it mechanistically to CS‐induced reduction of SIRT1. Targeted deletion of Bmal1 in lung epithelium augmented inflammation in response to CS, which was not attenuated by the selective SIRT1 activator SRT1720 (EC 50 =0.16 μM) in these mice. Thus, the circadian clock, specifically the enhancer BMAL1 in epithelium, plays a pivotal role, mediated by SIRT1‐dependent BMAL1, in the regulation of CS‐induced lung inflammatory and injurious responses.—Hwang, J.‐W., Sundar, I. K., Yao, H., Sellix, M. T., Rahman, I. Circadian clock function is disrupted by environmental tobacco/cigarette smoke, leading to lung inflammation and injury via a SIRT1‐BMAL1 pathway. FASEB J . 28, 176–194 (2014). www.fasebj.org
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Cites
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“SRT1720 (100 mg/kg, 95% pure by C-13 NMR and LCMS, synthesized by Life Chemicals, Niagara-on-the-Lake, ON, Canada) was administered to the acute air- and CS-exposed mice daily for 3 d through oral gavage 1 h before CS exposure (40).”
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Self-citationSIRT1 protects against emphysema via FOXO3-mediated reduction of premature senescence in mice
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Self-citationAn epithelial circadian clock controls pulmonary inflammation and glucocorticoid action
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SIRT1 protects against cigarette smoke-induced lung oxidative stress via a FOXO3-dependent mechanism
Yao, H., Sundar, I. K., Ahmad, T., Lerner, C., Gerloff, J., Friedman, A. E., Phipps, R. P., Sime, P. J., McBurney, M. W., Guarente, L., et al. (2014) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00323.2013 · Cited by 104
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Metadata
- Authors
- Hwang, J., Sundar, I. K., Yao, H., Sellix, M. T., & Rahman, I.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2013-09-11
- Volume
- 28
- Issue
- 1
- Pages
- 176-194
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2071794910
- Cited by
- 194
- References
- 11
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- green
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