ArticleClinical and experimental pharmacology & physiology2011
Overexpression of cationic amino acid transporter-1 increases nitric oxide production in hypoxic human pulmonary microvascular endothelial cells.
Article in Clinical and experimental pharmacology & physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- L-arginine and Its Derivatives Correlate with Exercise Capacity in Patients with Advanced Heart Failure.Biomolecules · 2023Article
- Reduced L-Arginine and L-Arginine-ADMA-Ratio, and Increased SDMA after Norseman Xtreme Triathlon.Sports (Basel, Switzerland) · 2021Article
- Differential effects of the Src family tyrosine kinases Yes and Fyn on lipopolysaccharide-induced lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Endothelial Dysfunction Driven by Hypoxia-The Influence of Oxygen Deficiency on NO Bioavailability.Biomolecules · 2021Review
- DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells.Physiological reports · 2019Article
- Deficiency of cationic amino acid transporter-2 protects mice from hyperoxia-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Can Co-Activation of Nrf2 and Neurotrophic Signaling Pathway Slow Alzheimer's Disease?International journal of molecular sciences · 2017Review
- Hypoxic proliferation requires EGFR-mediated ERK activation in human pulmonary microvascular endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Galectin-1 Reduces Neuroinflammation via Modulation of Nitric Oxide-Arginase Signaling in HIV-1 Transfected Microglia: a Gold Nanoparticle-Galectin-1 "Nanoplex" a Possible Neurotherapeutic?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017Article
- The Src family tyrosine kinases src and yes have differential effects on inflammation-induced apoptosis in human pulmonary microvascular endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies.Molecular neurobiology · 2016Review
- Asymmetric dimethylarginine does not inhibit arginase activity and is pro-proliferative in pulmonary endothelial cells.Clinical and experimental pharmacology & physiology · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
1. The endogenous production of and/or the bioavailability of nitric oxide (NO) is decreased in pulmonary hypertensive diseases. L-arginine (L-arg) is the substrate for NO synthase (NOS). L-arg is transported into cells via the cationic amino acid transporters (CAT), of which there are two isoforms in endothelial cells, CAT-1 and CAT-2. 2. To test the hypothesis that hypoxia will decrease CAT expression and L-arg uptake resulting in decreased NO production in human pulmonary microvascular endothelial cells (hPMVEC), cells were incubated in either normoxia (21% O(2), 5% CO(2), balance N(2)) or hypoxia (1% O(2), 5% CO(2), balance N(2)). 3. The hPMVEC incubated in hypoxia had 80% less NO production than cells incubated in normoxia (P < 0.01). The hPMVEC incubated in hypoxia had significantly lower CAT-2 mRNA levels than normoxic hPMVEC (P < 0.005), and the transport of L-arg was 40% lower in hypoxic than in normoxic hPMVEC (P < 0.01). In hypoxic cells, overexpression of CAT-1 resulted in significantly greater L-arg transport and NO production (P < 0.05). 4. These results demonstrate that in hPMVEC, hypoxia decreased CAT-2 expression, L-arg uptake and NO production. Furthermore, the hypoxia-induced decrease in NO production in hPMVEC can be attenuated by overexpressing CAT in these cells. We speculate that the CAT may represent a novel therapeutic target for treating pulmonary hypertensive disorders.
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