ArticleAmerican journal of physiology. Cell physiology2014
Effects of chronic exposure to cigarette smoke on canonical transient receptor potential expression in rat pulmonary arterial smooth muscle.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 49 citations in OpenAlex.
- Uncovering a novel role of nAChRs in oxidative stress-mediated vascular dysfunction in COPD.Redox biology · 2025Article
- The Potential Important Role of Mitochondrial Rieske Iron-Sulfur Protein as a Novel Therapeutic Target for Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease.Biomedicines · 2022Review
- Retinal Microvascular Reactivity in Chronic Cigarette Smokers and Non-smokers: An Observational Cross-Sectional Study.Frontiers in medicine · 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
- A novel rat model of pulmonary hypertension induced by mono treatment with SU5416.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells.International journal of molecular medicine · 2020Article
- Tetramethylpyrazine: A promising drug for the treatment of pulmonary hypertension.British journal of pharmacology · 2020Article
- Transient Receptor Potential Melastatin 8 (TRPM8)-Based Mechanisms Underlie Both the Cold Temperature-Induced Inflammatory Reactions and the Synergistic Effect of Cigarette Smoke in Human Bronchial Epithelial (16HBE) Cells.Frontiers in physiology · 2019Article
- Comparison and evaluation of two different methods to establish the cigarette smoke exposure mouse model of COPD.Scientific reports · 2017Article
- The Role of Transient Receptor Potential Channel 6 Channels in the Pulmonary Vasculature.Frontiers in immunology · 2017Review
- Effect of Cigarette Smoking on Epithelial to Mesenchymal Transition (EMT) in Lung Cancer.Journal of clinical medicine · 2016Review
- The Role of nAChR and Calcium Signaling in Pancreatic Cancer Initiation and Progression.Cancers · 2015Review
- Hypoxia inducible factor-1-dependent up-regulation of BMP4 mediates hypoxia-induced increase of TRPC expression in PASMCs.Cardiovascular research · 2015Article
- Activation of renin-angiotensin-aldosterone system (RAAS) in the lung of smoking-induced pulmonary arterial hypertension (PAH) rats.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2015Article
- Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats.Acta pharmacologica Sinica · 2015Article
- The role of inflammation in hypoxic pulmonary hypertension: from cellular mechanisms to clinical phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- NOX4 mediates BMP4-induced upregulation of TRPC1 and 6 protein expressions in distal pulmonary arterial smooth muscle cells.PloS one · 2014Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
To clarify the possible mechanism of cigarette smoke (CS)-induced pulmonary hypertension and furthermore provide effective targets for prevention and treatment, the effects of chronic CS on rat pulmonary arterial smooth muscle in vivo and nicotine treatment on rat pulmonary arterial smooth muscle cells (PASMCs) in vitro were investigated. In this study, we demonstrated that chronic CS exposure led to rat weight loss, right ventricular hypertrophy, and pulmonary arterial remodeling. A fluorescence microscope was used to measure intracellular calcium concentration ([Ca(2+)]i) in rat distal PASMCs. Results showed that basal [Ca(2+)]i and store-operated calcium entry (SOCE) levels in PASMCs from 3- and 6-mo CS-exposed rats were markedly higher than those in cells from the unexposed control animals (the increases in 6-mo CS group were more significant than that in 3-mo group), accompanied with increased canonical transient receptor potential 1 (TRPC1) and TRPC6 expression at both mRNA and protein levels in isolated distal PA. Simultaneously, in vitro study showed that nicotine treatment (10 nM) significantly increased basal [Ca(2+)]i and SOCE and upregulated TRPC1 and TRPC6 expression in cultured rat distal PASMCs. TRPC siRNA knockdown strategies revealed that the elevations of basal [Ca(2+)]i and SOCE induced by nicotine in PASMCs were TRPC1 and TRPC6 dependent. These results suggested that chronic CS-induced changes in vascular tone and structure in PA and the development of pulmonary hypertension might be largely due to upregulation of TRPC1 and TRPC6 expression in PASMCs, in which nicotine played an important role.
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