ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Activation of hypoxia-inducible factor-1 in pulmonary arterial smooth muscle cells by endothelin-1.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 73 citations in OpenAlex.
- Temporal Coordination of Angiogenic, Nitric Oxide, and Endothelin Pathways in Vascular Adaptation to Hypoxia and Reoxygenation.Cardiovascular drugs and therapy · 2026Review
- Changes in Macrophages in Pulmonary Hypertension: A Focus on High-altitude Pulmonary Hypertension.Anatolian journal of cardiology · 2025Review
- Enhanced glycolysis causes extracellular acidification and activates acid-sensing ion channel 1a in hypoxic pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Histone lactylation driven by mROS-mediated glycolytic shift promotes hypoxic pulmonary hypertension.Journal of molecular cell biology · 2023Article
- On the mechanisms underlying activation and reversal of high altitude-induced pulmonary hypertension in humans - Another piece in the pulmonary puzzle.Experimental physiology · 2023Article
- Effects of Acute Hypobaric Hypoxia Exposure on Cardiovascular Function in Unacclimatized Healthy Subjects: A "Rapid Ascent" Hypobaric Chamber Study.International journal of environmental research and public health · 2022Article
- Differential response to hypoxia in leiomyoma and myometrial cells.Life sciences · 2022Article
- Article
- Hypoxia Inducible Factors as Central Players in the Pathogenesis and Pathophysiology of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Hypoxia-inducible factor signaling in pulmonary hypertension.The Journal of clinical investigation · 2020Review
- Cellular Pathways Promoting Pulmonary Vascular Remodeling by Hypoxia.Physiology (Bethesda, Md.) · 2020Review
- World health days in May 2020: pulmonary hypertension; asthma; and tobacco-, smoking-, and vaping-related disease in focus.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Metabolism and Redox in Pulmonary Vascular Physiology and Pathophysiology.Antioxidants & redox signaling · 2019Review
- A RASSF1A-HIF1α loop drives Warburg effect in cancer and pulmonary hypertension.Nature communications · 2019Article
- Revisiting the role of hypoxia-inducible factors in pulmonary hypertension.Current opinion in physiology · 2019Article
- Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Rho kinase and NaPhysiological reports · 2018Article
- Reactive oxygen species induced CaAmerican journal of physiology. Lung cellular and molecular physiology · 2018Article
- Aquaporin 1-mediated changes in pulmonary arterial smooth muscle cell migration and proliferation involve β-catenin.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Protein kinase Cα stimulates hypoxia‑induced pulmonary artery smooth muscle cell proliferation in rats through activating the extracellular signal‑regulated kinase 1/2 pathway.Molecular medicine reports · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Numerous cellular responses to hypoxia are mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1). HIF-1 plays a central role in the pathogenesis of hypoxic pulmonary hypertension. Under certain conditions, HIF-1 may utilize feedforward mechanisms to amplify its activity. Since hypoxia increases endothelin-1 (ET-1) levels in the lung, we hypothesized that during moderate, prolonged hypoxia ET-1 might contribute to HIF-1 signaling in pulmonary arterial smooth muscle cells (PASMCs). Primary cultures of rat PASMCs were treated with ET-1 or exposed to moderate, prolonged hypoxia (4% O(2) for 60 h). Levels of the oxygen-sensitive HIF-1α subunit and expression of HIF target genes were increased in both hypoxic cells and cells treated with ET-1. Both hypoxia and ET-1 also increased HIF-1α mRNA expression and decreased mRNA and protein expression of prolyl hydroxylase 2 (PHD2), which is the protein responsible for targeting HIF-1α for O(2)-dependent degradation. The induction of HIF-1α by moderate, prolonged hypoxia was blocked by BQ-123, an antagonist of ET-1 receptor subtype A. The effects of ET-1 were mediated by increased intracellular calcium, generation of reactive oxygen species, and ERK1/2 activation. Neither ET-1 nor moderate hypoxia induced the expression of HIF-1α or HIF target genes in aortic smooth muscle cells. These results suggest that ET-1 induces a PASMC-specific increase in HIF-1α levels by upregulation of HIF-1α synthesis and downregulation of PHD2-mediated degradation, thereby amplifying the induction of HIF-1α in PASMCs during moderate, prolonged hypoxia.
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