ArticleAmerican journal of respiratory cell and molecular biology2009
RelB is differentially regulated by IkappaB Kinase-alpha in B cells and mouse lung by cigarette smoke.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.Cell communication and signaling : CCS · 2025Article
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
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- Hexavalent chromium exposure activates the non-canonical nuclear factor kappa B pathway to promote immune checkpoint protein programmed death-ligand 1 expression and lung carcinogenesis.Cancer letters · 2024Article
- Testosterone attenuates pulmonary epithelial inflammation in male rats of COPD model through preventing NRF1-derived NF-κB signaling.Journal of molecular cell biology · 2021Article
- Whole-Exome Sequencing Implicates theFrontiers in cell and developmental biology · 2021Article
- Overview on Interactive Role of Inflammation, Reactive Oxygen Species, and Calcium Signaling in Asthma, COPD, and Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- Innate Immune Responses and Pulmonary Diseases.Advances in experimental medicine and biology · 2021Article
- Fisetin-treatment alleviates airway inflammation through inhbition of MyD88/NF-κB signaling pathway.International journal of molecular medicine · 2018Article
- Blockade of RAGE ameliorates elastase-induced emphysema development and progressionFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- NF-kappaB Signaling in Chronic Inflammatory Airway Disease.Biomolecules · 2015Review
- Bronchial airway gene expression in smokers with lung or head and neck cancer.Cancer medicine · 2014Article
- Paracrine potential of fibroblasts exposed to cigarette smoke extract with vascular growth factor induction.The Laryngoscope · 2013Article
- Oxidative stress and chromatin remodeling in chronic obstructive pulmonary disease and smoking-related diseases.Antioxidants & redox signaling · 2013Review
- Effects of cigarette smoke extract on primary activated T cells.Cellular immunology · 2013Article
- Adverse effects of wood smoke PM(2.5) exposure on macrophage functions.Inhalation toxicology · 2013Article
- Mitogen- and stress-activated kinase 1 (MSK1) regulates cigarette smoke-induced histone modifications on NF-κB-dependent genes.PloS one · 2012Article
- Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease.Toxicology and applied pharmacology · 2011Review
- Article
- Protein kinase C zeta mediates cigarette smoke/aldehyde- and lipopolysaccharide-induced lung inflammation and histone modifications.The Journal of biological chemistry · 2010Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
The activation of transcription factor NF-kappaB is controlled by two main pathways: the classical canonical (RelA/p65-p50)- and the alternative noncanonical (RelB/p52)-NF-kappaB pathways. RelB has been shown to play a protective role in RelA/p65-mediated proinflammatory cytokine release in immune-inflammatory lymphoid cells. Increased infiltration of macrophages and lymphoid cells occurs in lungs of patients with chronic obstructive pulmonary disease, leading to abnormal inflammation. We hypothesized that RelB, and its signaling pathway, is differentially regulated in macrophages and B cells and in lung cells, leading to differential regulation of proinflammatory cytokines in response to cigarette smoke (CS). CS exposure increased the levels of RelB and NF-kappaB-inducing kinase associated with recruitment of RelB on promoters of the IL-6 and macrophage inflammatory protein-2 genes in mouse lung. Treatment of macrophage cell line, MonoMac6, with CS extract showed activation of RelB. In contrast, RelB was degraded by a proteasome-dependent mechanism in B lymphocytes (human Ramos, mouse WEHI-231, and primary mouse spleen B cells), suggesting that RelB is differentially regulated in lung inflammatory and lymphoid cells in response to CS exposure. Transient transfection of dominant negative IkappaB-kinase-alpha and double mutants of NF-kappaB-inducing kinase partially attenuated the CS extract-mediated loss of RelB in B cells and normalized the increased RelB level in macrophages. Taken together, these data suggest that RelB is differentially regulated in response to CS exposure in macrophages, B cells, and in lung cells by IkappaB-kinase-alpha-dependent mechanism. Rapid degradation of RelB signals for RelA/p65 activation and loss of its protective ability to suppress the proinflammatory cytokine release in lymphoid B cells.
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