ArticlePflugers Archiv : European journal of physiology2016
Effect of hypoxia on TRPV1 and TRPV4 channels in rat pulmonary arterial smooth muscle cells.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 76 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Integrative Genomics and Multi-Tissue Transcriptomics Identify Key Loci and Pathways for Hypoxia Tolerance in Grass Carp.Animals : an open access journal from MDPI · 2025Article
- The role of TRPA1 in lung cancer.Translational lung cancer research · 2025Review
- Review
- Pathophysiology of Group 3 Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxia.International journal of molecular sciences · 2025Review
- Calcitonin gene‑related peptide alleviates hyperoxia‑induced human alveolar cell injury via the CGRPR/TRPV1/Ca2Molecular medicine reports · 2024Article
- Neutrophil extracellular traps promote proliferation of pulmonary smooth muscle cells mediated by CCDC25 in pulmonary arterial hypertension.Respiratory research · 2024Article
- Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models.Channels (Austin, Tex.) · 2023Review
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Hypoxia augments TRPM3-mediated calcium influx in vagal sensory neurons.Autonomic neuroscience : basic & clinical · 2023Article
- Review
- Bidirectional TRP/L Type CaBiomolecules · 2023Article
- A modified primary culture method of rat pulmonary vein smooth muscle cells.Journal of cardiothoracic surgery · 2023Article
- Cell Confluence Modulates TRPV4 Channel Activity in Response to Hypoxia.Biomolecules · 2022Article
- CaInternational journal of molecular sciences · 2022Review
- NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction.Antioxidants (Basel, Switzerland) · 2022Article
- Effects of FW2 Nanoparticles Toxicity in a New In Vitro Pulmonary Vascular Cells Model Mimicking Endothelial Dysfunction.Cardiovascular toxicology · 2022Article
- Effects of Ion-Transporting Proteins on the Digestive System Under Hypoxia.Frontiers in physiology · 2022Review
- Mechanosensitivity in Pulmonary Circulation: Pathophysiological Relevance of Stretch-Activated Channels in Pulmonary Hypertension.Biomolecules · 2021Review
- Ion channels as convergence points in the pathology of pulmonary arterial hypertension.Biochemical Society transactions · 2021Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient receptor potential (TRP) channels of the vanilloid subfamily, mainly TRPV1 and TRPV4, are expressed in pulmonary artery smooth muscle cells (PASMC) and implicated in the remodeling of pulmonary artery, a landmark of pulmonary hypertension (PH). Among a variety of PH subtypes, PH of group 3 are mostly related to a prolonged hypoxia exposure occurring in a variety of chronic lung diseases. In the present study, we thus investigated the role of hypoxia on TRPV1 and TRPV4 channels independently of the increased pulmonary arterial pressure that occurs during PH. We isolated PASMC from normoxic rat and cultured these cells under in vitro hypoxia. Using microspectrofluorimetry and the patch-clamp technique, we showed that hypoxia (1 % O2 for 48 h) significantly increased stretch- and TRPV4-induced calcium responses. qRT-PCR, Western blotting, and immunostaining experiments revealed that the expression of TRPV1 and TRPV4 was not enhanced under hypoxic conditions, but we observed a membrane translocation of TRPV1. Furthermore, hypoxia induced a reorganization of the F-actin cytoskeleton, the tubulin, and intermediate filament networks (immunostaining experiments), associated with an enhanced TRPV1- and TRPV4-induced migratory response (wound-healing assay). Finally, as assessed by immunostaining, exposure to in vitro hypoxia elicited a significant increase in NFATc4 nuclear localization. Cyclosporin A and BAPTA-AM inhibited NFATc4 translocation, indicating the activation of the Ca(2+)/calcineurin/NFAT pathway. In conclusion, these data point out the effect of hypoxia on TRPV1 and TRPV4 channels in rat PASMC, suggesting that these channels can act as direct signal transducers in the pathophysiology of PH.
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