SIRT1, an antiinflammatory and antiaging protein, is decreased in lungs of patients with chronic obstructive pulmonary disease
Open accessAbstract
Rationale: Abnormal inflammation and accelerated decline in lung function occur in patients with chronic obstructive pulmonary disease (COPD). Human sirtuin (SIRT1), an antiaging and antiinflammatory protein, is a metabolic NAD+-dependent protein/histone deacetylase that regulates proinflammatory mediators by deacetylating histone and nonhistone proteins. Objectives: To determine the expression of SIRT1 in lungs of smokers and patients with COPD, and to elucidate the regulation of SIRT1 in response to cigarette smoke in macrophages, and its impact on nuclear factor (NF)-κB regulation. Methods: SIRT1 and NF-κB levels were assessed in lung samples of nonsmokers, smokers, and patients with COPD. Human monocyte–macrophage cells (MonoMac6) were treated with cigarette smoke extract (CSE) to determine the mechanism of CSE-mediated regulation of SIRT1 and its involvement in RelA/p65 regulation and IL-8 release. Measurements and Main Results: Peripheral lungs of smokers and patients with COPD showed decreased levels of nuclear SIRT1, as compared with nonsmokers, associated with its post-translational modifications (formation of nitrotyrosine and aldehyde carbonyl adducts). Treatment of MonoMac6 cells with CSE showed decreased levels of SIRT1 associated with increased acetylation of RelA/p65 NF-κB. Mutation or knockdown of SIRT1 resulted in increased acetylation of nuclear RelA/p65 and IL-8 release, whereas overexpression of SIRT1 decreased IL-8 release in response to CSE treatment in MonoMac6 cells. Conclusions: SIRT1 levels were reduced in macrophages and lungs of smokers and patients with COPD due to its post-translational modifications by cigarette smoke–derived reactive components, leading to increased acetylation of RelA/p65. Thus, SIRT1 plays a pivotal role in regulation of NF-κB–dependent proinflammatory mediators in lungs of smokers and patients with COPD.
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Exposure to cigarette smoke oxidatively decreases SIRT1 levels and concomitantly increases NF-κB-dependent release of pro-inflammatory mediators in MonoMac6 cells and in mouse lungs.
“Exposure to cigarette smoke oxidatively decreases SIRT1 levels and concomitantly increases NF-κB-dependent release of pro-inflammatory mediators in MonoMac6 cells and in mouse lungs [198], [199].”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [199]
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- Authors
- Rajendrasozhan, S., Yang, S.-R., Kinnula, V. L., & Rahman, I.
- Affiliations
- University of Rochester Medicine (US)
- University of Helsinki (FI)
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-04
- Volume
- 177
- Issue
- 8
- Pages
- 861-870
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- PMC
- PMC2292827
- OpenAlex
- W2123193437
- Cited by
- 520
- References
- 49
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 19 · 2023: 28 · 2022: 20 · 2021: 27 · 2020: 33 · 2019: 29 · 2018: 28 · 2017: 34 · 2016: 29 · 2015: 35 · 2014: 30 · 2013: 37 · 2012: 37
- FWCI
- 13.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Funders
- Pfizer
- National Institute of Environmental Health Sciences (ES-01247, P30ES001247)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- SIRT1, chronic obstructive pulmonary disease, cigarette smoke, NF-κB, macrophages, interleukin-8, nitrotyrosine, post-translational modification, inflammation, aging, smokers
- MeSH terms
- Acetylation, Adult, Aged, Female, Humans, Macrophages, Male, Middle Aged, Protein Processing, Post-Translational, Smoke, Smoking, Nicotiana, Pulmonary Disease, Chronic Obstructive, Sirtuins, Cell Line, Tumor, Sirtuin 1
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