ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Inhibition of mTOR attenuates store-operated Ca2+ entry in cells from endarterectomized tissues of patients with chronic thromboembolic pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 61 citations in OpenAlex.
- The Role of the Pulmonary Vascular Microenvironment in Chronic Thromboembolic Pulmonary Hypertension.Pulmonary circulation · 2025Review
- ANO1, CaV1.2, and IP3R form a localized unit of EC-coupling in mouse pulmonary arterial smooth muscle.The Journal of general physiology · 2023Article
- Antiproliferative effect of selexipag active metabolite MRE-269 on pulmonary arterial smooth muscle cells from patients with chronic thromboembolic pulmonary hypertension.Pulmonary circulation · 2023Article
- Article
- Protein network analyses of pulmonary endothelial cells in chronic thromboembolic pulmonary hypertension.Scientific reports · 2021Article
- mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target.International journal of molecular sciences · 2021Review
- Effect of EZH2 on pulmonary artery smooth muscle cell migration in pulmonary hypertension.Molecular medicine reports · 2021Article
- AMPKα2 deficiency exacerbates hypoxia-induced pulmonary hypertension by promoting pulmonary arterial smooth muscle cell proliferation.Journal of physiology and biochemistry · 2020Article
- Notch3 signalling and vascular remodelling in pulmonary arterial hypertension.Clinical science (London, England : 1979) · 2019Review
- Triple negative breast cancer: shedding light onto the role of pi3k/akt/mtor pathway.Oncotarget · 2016Review
- Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Upregulation of canonical transient receptor potential channel in the pulmonary arterial smooth muscle of a chronic thromboembolic pulmonary hypertension rat model.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- Chronic thromboembolic pulmonary hypertension: a distinct disease entity.European respiratory review : an official journal of the European Respiratory Society · 2015Review
- Article
- Inhibition of Excessive Cell Proliferation by Calcilytics in Idiopathic Pulmonary Arterial Hypertension.PloS one · 2015Article
- PK10453, a nonselective platelet-derived growth factor receptor inhibitor, prevents the progression of pulmonary arterial hypertension.Pulmonary circulation · 2014Article
- Article
- Thrombin-mediated activation of Akt signaling contributes to pulmonary vascular remodeling in pulmonary hypertension.Physiological reports · 2013Article
- Long-term mTOR inhibitors administration evokes altered calcium homeostasis and platelet dysfunction in kidney transplant patients.Journal of cellular and molecular medicine · 2013Article
- mTOR and vascular remodeling in lung diseases: current challenges and therapeutic prospects.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary vascular remodeling occurs in patients with chronic thromboembolic pulmonary hypertension (CTEPH). One factor contributing to this vascular wall thickening is the proliferation of pulmonary artery smooth muscle cells (PASMC). Store-operated Ca(2+) entry (SOCE) and cytosolic free Ca(2+) concentration ([Ca(2+)](cyt)) in PASMC are known to be important in cell proliferation and vascular remodeling in pulmonary hypertension. Rapamycin is widely known for its antiproliferative effects in injured coronary arteries. Although several reports have suggested favorable effects of rapamycin in animal models of pulmonary hypertension, no reports have been published to date in human tissues. Here we report that rapamycin has an inhibitory effect on SOCE and an antiproliferative effect on PASMC derived from endarterectomized tissues of CTEPH patients. Cells were isolated from endarterectomized tissues obtained from patients undergoing pulmonary thromboendarterectomy (PTE). Immunohistochemical analysis indicated high deposition of platelet-derived growth factor (PDGF) in tissue sections from PTE tissues and increased PDGF receptor expression. PDGF transiently phosphorylated Akt, mammalian target of rapamycin (mTOR), and p70S6 kinase in CTEPH cells from CTEPH patients. Acute treatment (30 min) with rapamycin (10 nM) slightly increased cyclopiazonic acid (10 microM)-induced Ca(2+) mobilization and significantly reduced SOCE. Chronic treatment (24 h) with rapamycin reduced Ca(2+) mobilization and markedly inhibited SOCE. The inhibitory effects of rapamycin on SOCE were less prominent in control cells. Rapamycin also significantly reduced PDGF-stimulated cell proliferation. In conclusion, the data from this study indicate the importance of the mTOR pathway in the development of pulmonary vascular remodeling in CTEPH and suggest a potential therapeutic benefit of rapamycin (or inhibition of mTOR) in these patients.
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