ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPKα
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. 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.
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Role of Arginase-II in Podocyte Injury under Hypoxic Conditions.Biomolecules · 2022Article
- Hypoxic pulmonary endothelial cells release epidermal growth factor leading to vascular smooth muscle cell arginase-2 expression and proliferation.Physiological reports · 2022Article
- AMPK and Pulmonary Hypertension: Crossroads Between Vasoconstriction and Vascular Remodeling.Frontiers in cell and developmental biology · 2021Review
- Arginase as a Potential Biomarker of Disease Progression: A Molecular Imaging Perspective.International journal of molecular sciences · 2020Review
- AMPK Enhances Transcription of Selected Nrf2 Target Genes via Negative Regulation of Bach1.Frontiers in cell and developmental biology · 2020Article
- Polyamines in mammalian pathophysiology.Cellular and molecular life sciences : CMLS · 2019Review
- Role of Arginase 2 in Systemic Metabolic Activity and Adipose Tissue Fatty Acid Metabolism in Diet-Induced Obese Mice.International journal of molecular sciences · 2019Article
- Macrophage-Derived IL1β and TNFα Regulate Arginine Metabolism in Neuroblastoma.Cancer research · 2019Article
- Hypoxia Enhances Endothelial Intercellular Adhesion Molecule 1 Protein Level Through Upregulation of Arginase Type II and Mitochondrial Oxidative Stress.Frontiers in physiology · 2019Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Hypoxic-induction of arginase II requires EGF-mediated EGFR activation in human pulmonary microvascular endothelial cells.Physiological reports · 2018Article
- Arginase: A Multifaceted Enzyme Important in Health and Disease.Physiological reviews · 2018Review
- The Arginase Pathway in Neonatal Brain Hypoxia-Ischemia.Developmental neuroscience · 2018Review
- The role and mechanism of AMPK in pulmonary hypertension.Therapeutic advances in respiratory diseaseReview
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Pulmonary artery smooth muscle cell (PASMC) proliferation is one of the hallmark features of hypoxia-induced pulmonary hypertension. With only supportive treatment options available for this life-threatening disease, treating and preventing the proliferation of PASMCs is a viable therapeutic option. A key promoter of hypoxia-induced increases in the number of viable human PASMCs is arginase II, with attenuation of viable cell numbers following pharmacologic inhibition or siRNA knockdown of the enzyme. Additionally, increased levels of arginase have been demonstrated in the pulmonary vasculature of patients with pulmonary hypertension. The signaling pathways responsible for the hypoxic induction of arginase II in PASMCs, however, remain unknown. Hypoxia is a recognized activator of AMPK, which is known to be expressed in human PASMCs (hPASMCs). Activation of AMPK by hypoxia has been shown to promote cell survival in PASMCs. In addition, pharmacologic agents targeting AMPK have been shown to attenuate chronic hypoxia-induced pulmonary hypertension in animal models. The present studies tested the hypothesis that hypoxia-induced arginase II expression in hPASMCs is mediated through AMPK signaling. We found that pharmacologic inhibitors of AMPK, as well as siRNA knockdown of AMPKα1, prevented hypoxia-induced arginase II. The hypoxia-induced increase in viable hPASMC numbers was also prevented following both pharmacologic inhibition and siRNA knockdown of AMPK. Furthermore, we demonstrate that overexpression of AMPK induced arginase II protein expression and viable cells numbers in hPASMCs.
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