ArticleJournal of neuroinflammation2011
Cigarette smoke extract upregulates heme oxygenase-1 via PKC/NADPH oxidase/ROS/PDGFR/PI3K/Akt pathway in mouse brain endothelial cells.
Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Exercise and smoking: health rivals revealing shared protective mechanisms in Parkinson's?NPJ Parkinson's disease · 2026Review
- Eucalyptus Wood Smoke Extract Elicits a Dose-Dependent Effect in Brain Endothelial Cells.International journal of molecular sciences · 2024Article
- Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review.Antioxidants (Basel, Switzerland) · 2023Review
- Compound K ameliorates airway inflammation and mucus secretion through the regulation of PKC signaling in vitro and in vivo.Journal of ginseng research · 2022Article
- D609 inhibition of phosphatidylcholine-specific phospholipase C attenuates prolonged insulin stimulation-mediated GLUT4 downregulation in 3T3-L1 adipocytes.Journal of physiology and biochemistry · 2022Article
- Induction of Heme Oxygenase-1 by 15d-Prostaglandin JAntioxidants (Basel, Switzerland) · 2022Article
- 5,8-Dihydroxy-4 ', 7-dimethoxyflavone Attenuates TNF-Oxidative medicine and cellular longevity · 2022Article
- Oxidative Inactivation of the Proteasome Augments Alveolar Macrophage Secretion of Vesicular SOCS3.Cells · 2020Article
- Adaptive Potential of the Heme Oxygenase/Carbon Monoxide Pathway During Hypoxia.Frontiers in physiology · 2020Article
- Inhibition of stress fiber formation preserves blood-brain barrier after intracerebral hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Immune-regulating effects of exercise on cigarette smoke-induced inflammation.Journal of inflammation research · 2018Review
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma.Oral oncology · 2017Article
- Transforming growth factor β1 enhances heme oxygenase 1 expression in human synovial fibroblasts by inhibiting microRNA 519b synthesis.PloS one · 2017Article
- Isoegomaketone Upregulates Heme Oxygenase-1 in RAW264.7 Cells via ROS/p38 MAPK/Nrf2 Pathway.Biomolecules & therapeutics · 2016Article
- Article
- Urotensin-II-Mediated Reactive Oxygen Species Generation via NADPH Oxidase Pathway Contributes to Hepatic Oval Cell Proliferation.PloS one · 2015Article
- Article
- Proinflammatory responses of heme in alveolar macrophages: repercussion in lung hemorrhagic episodes.Mediators of inflammation · 2013Article
- MiR-101 and miR-144 regulate the expression of the CFTR chloride channel in the lung.PloS one · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the brain, the inducible form of heme oxygenase (HO-1) has been recently demonstrated to exacerbate early brain injury produced by intracerebral hemorrhagic stroke which incident rate has been correlated with cigarette smoking previously. Interestingly, cigarette smoke (CS) or chemicals present in CS have been shown to induce HO-1 expression in various cell types, including cerebral endothelial cells. However, the mechanisms underlying CS modulating HO-1 protein expression are not completely understood in the brain vessels.
objectiveThe aim of the present study was to investigate the mechanisms underlying CS modulating HO-1 protein expression in cerebral endothelial cells.
methodsCultured cerebral endothelial cells (bEnd.3) were used to investigate whether a particulate phase of cigarette smoke extract (PPCSE) regulates HO-1 expression and to investigate the molecular mechanisms involved in HO-1 expression in bEnd.3 cells.
resultsWe demonstrated that PPCSE (30 μg/ml) significantly induced HO-1 protein expression and its enzymatic activity in bEnd.3 cells determined by western blotting and bilirubin formation, respectively. PPCSE-induced HO-1 expression was mediated through phosphatidylcholine phospholipase C (PC-PLC), PKCδ, and PI3K/Akt which were observed by pretreatment with their respective pharmacological inhibitors or transfection with dominant negative mutants of PKCδ and Akt. ROS scavenger (N-acetyl-L-cysteine, NAC) blocked the PPCSE-induced ROS generation and HO-1 expression. Pretreatment with selective inhibitors of PKCδ (rottlerin) and NADPH oxidase [diphenyleneiodonium chloride (DPI) and apocynin (APO)] attenuated the PPCSE-induced NADPH oxidase activity, ROS generation, and HO-1 expression. In addition, we found that PPCSE induced PI3K/Akt activation via NADPH oxidase/ROS-dependent PDGFR phosphorylation.
conclusionsTaken together, these results suggested that PPCSE-induced HO-1 expression is mediated by a PC-PLC/PKCδ/NADPH oxidase-dependent PDGFR/PI3K/Akt pathway in bEnd.3 cells.
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