ArticleAmerican journal of respiratory cell and molecular biology2012
Pharmacologic agents elevating cAMP prevent arginase II expression and proliferation of pulmonary artery smooth muscle cells.
Article in American journal of respiratory cell and molecular biology, 2012. 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, 27 citations in OpenAlex.
- Pde3a and Pde3b regulation of murine pulmonary artery smooth muscle cell growth and metabolism.Physiological reports · 2024Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Elevated serum extracellular vesicle arginase 1 in type 2 diabetes mellitus: a cross-sectional study in middle-aged and elderly population.BMC endocrine disorders · 2022Article
- Modulation of Arginase-2 mRNA Levels byJournal of lipids · 2022Article
- Nitric oxide activates AMPK by modulating PDE3A in human pulmonary artery smooth muscle cells.Physiological reports · 2020Article
- The Role of Regulatory T Cells in Pulmonary Arterial Hypertension.Journal of the American Heart Association · 2019Review
- Hypoxic-induction of arginase II requires EGF-mediated EGFR activation in human pulmonary microvascular endothelial cells.Physiological reports · 2018Article
- Arginase Inhibition Reverses Monocrotaline-Induced Pulmonary Hypertension.International journal of molecular sciences · 2017Article
- Hypoxic proliferation requires EGFR-mediated ERK activation in human pulmonary microvascular endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPKαAmerican journal of physiology. Lung cellular and molecular physiology · 2017Article
- An arginase-1 SNP that protects against the development of pulmonary hypertension in bronchopulmonary dysplasia enhances NO-mediated apoptosis in lymphocytes.Physiological reports · 2016Article
- Regulatory T cells in cardiovascular diseases.Nature reviews. Cardiology · 2016Review
- Resveratrol prevents hypoxia-induced arginase II expression and proliferation of human pulmonary artery smooth muscle cells via Akt-dependent signaling.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Thioredoxin-1 mediates hypoxia-induced pulmonary artery smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Arginase: the emerging therapeutic target for vascular oxidative stress and inflammation.Frontiers in immunology · 2013Article
- Role of arginase in vessel wall remodeling.Frontiers in immunology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Arginase II has been shown to be involved in the hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (hPASMCs). The signal transduction pathways responsible for the induction of arginase II are poorly understood. Cyclic AMP is involved in many intracellular processes, and cAMP levels are regulated by a balance between production via adenylate cyclases and degradation via phosphodiesterases. The purpose of this study was to determine the effects of cAMP on hypoxia-induced arginase expression, activity, and proliferation in hPASMCs. We found that the cAMP analog 8-Bromo-cAMP (8-Br-cAMP), the adenylate cyclase activator forskolin, and the phosphodiesterase 3 inhibitor cilostamide prevented the hypoxic induction of arginase II mRNA and protein expression in hPASMCs. The inhibition of arginase II protein was found to be mediated by exchange protein directly activated by cAMP. Arginase activity was decreased by 8-Br-cAMP, as evidenced by significantly lower V(max) for arginase in normoxia and hypoxia. The hypoxia-induced hPASMC proliferation was completely prevented by the addition of 8-Br-cAMP, forskolin, or cilostamide. These data are the first to describe the inhibitory effect of cAMP on arginase activity, expression, and resultant proliferation of hypoxic hPASMCs.
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