ArticleFrontiers in physiology2013
STAT3 modulates cigarette smoke-induced inflammation and protease expression.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- STAT3 and STAT6 activation in lung tissues correlates with inflammatory and clinical traits in COPD.ERJ open research · 2026Article
- Article
- The miR-876-5p/SOCS4/STAT3 pathway induced the expression of PD-L1 and suppressed antitumor immune responses.Cancer cell international · 2025Article
- Alpha-7 Nicotinic Receptor Agonist Protects Mice Against Pulmonary Emphysema Induced by Elastase.Inflammation · 2024Article
- Article
- The Role and Mechanism of Metformin in Inflammatory Diseases.Journal of inflammation research · 2023Review
- Impact of JAK/STAT inhibitors on human monocyte-derived-macrophages stimulated by cigarette smoke extract and lipopolysaccharide.Clinical and experimental pharmacology & physiology · 2022Article
- The Lung Alveolar Cell (LAC) miRNome and Gene Expression Profile of the SP-A-KO Mice After Infection With and Without Rescue With Human Surfactant Protein-A2 (1AFrontiers in immunology · 2022Article
- Evaluation of selected IL6/STAT3 pathway molecules and miRNA expression in chronic obstructive pulmonary disease.Scientific reports · 2021Article
- Long-term endogenous acetylcholine deficiency potentiates pulmonary inflammation in a murine model of elastase-induced emphysema.Scientific reports · 2021Article
- Effects of cigarette smoke extract on bronchial epithelial cells stimulated with Cryptococcus neoformans.Medical microbiology and immunology · 2021Article
- The Role of ABC Transporters in Lipid Metabolism and the Comorbid Course of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2021Review
- Current Understanding of the Immunomodulatory Activities of High-Density Lipoproteins.Biomedicines · 2021Review
- Participation of ABCA1 Transporter in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- High Dimensional Analyses of Circulating Immune Cells in Psoriatic Arthritis Detects Elevated Phosphorylated STAT3.Frontiers in immunology · 2021Article
- Differential Sex-Dependent Regulation of the Alveolar Macrophage miRNome of SP-A2 and co-ex (SP-A1/SP-A2) and Sex Differences Attenuation after 18 h of Ozone Exposure.Antioxidants (Basel, Switzerland) · 2020Article
- MiR-944/CISH mediated inflammation via STAT3 is involved in oral cancer malignance by cigarette smoking.Neoplasia (New York, N.Y.) · 2020Article
- Regulation of ATP binding cassette transporter A1 (ABCA1) expression: cholesterol-dependent and - independent signaling pathways with relevance to inflammatory lung disease.Respiratory research · 2020Review
- Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways.Free radical biology & medicine · 2020Article
- Cerebrovascular and Neurological Dysfunction under the Threat of COVID-19: Is There a Comorbid Role for Smoking and Vaping?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Signal transducer and activator of transcription-3 (STAT3) regulates inflammation, apoptosis, and protease expression, which are critical processes associated with airway injury and lung tissue destruction. However, the precise role of STAT3 in the development of airway diseases such as chronic obstructive pulmonary disease (COPD) has not been established. This study shows that cigarette smoke activates STAT3 in the lungs of mice. Since cigarette smoke activated STAT3 in the lung, we then evaluated how the loss of STAT3 would impact on smoke-mediated lung inflammation, protease expression, and apoptosis. STAT3(+/+) and STAT3(-/-) mice were exposed to 8 days of cigarette smoke. Compared to the STAT3(+/+) mice bronchoalveolar lavage fluid (BALF) cellularity was significantly elevated in the STAT3(-/-) mice both before and after cigarette smoke exposure, with the increase in cells primarily macrophages. In addition, smoke exposure induced significantly higher BALF protein levels of Interleukin-1α (IL-1α), and monocyte chemotactic protein-1 (MCP-1) and higher tissue expression of keratinocyte chemoattractant (KC) in the STAT3(-/-) mice. Lung mRNA expression of MMP-12 was increased in STAT3(-/-) at baseline. However, the smoke-induced increase in MMP-10 expression seen in the STAT3(+/+) mice was not observed in the STAT3(-/-) mice. Moreover, lung protein levels of the anti-inflammatory proteins SOCS3 and IL-10 were markedly lower in the STAT3(-/-) mice compared to the STAT3(+/+) mice. Lastly, apoptosis, as determined by caspase 3/7 activity assay, was increased in the STAT3(-/-) at baseline to levels comparable to those observed in the smoke-exposed STAT3(+/+) mice. Together, these results indicate that the smoke-mediated induction of lung STAT3 activity may play a critical role in maintaining normal lung homeostasis and function.
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