ArticleThe Journal of biological chemistry2012
Transient receptor potential canonical channels are required for in vitro endothelial tube formation.
Article in The Journal of biological chemistry, 2012. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed.
- TRPC channels contribute to endothelial dysfunction in pulmonary arterial hypertension.Respiratory research · 2025Article
- Review
- Peptide Lv and Angiogenesis: A Newly Discovered Angiogenic Peptide.Biomedicines · 2024Review
- A TRP to Pathological Angiogenesis and Vascular Normalization.Comprehensive Physiology · 2024Review
- CaBiomolecules · 2023Article
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- The transient receptor potential channels in rheumatoid arthritis: Need to pay more attention.Frontiers in immunology · 2023Review
- Transient Receptor Potential (TRP) Channels in Tumor Vascularization.International journal of molecular sciences · 2022Review
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Role of Ion Channel Remodeling in Endothelial Dysfunction Induced by Pulmonary Arterial Hypertension.Biomolecules · 2022Review
- Endothelial Transient Receptor Potential Canonical Channel Regulates Angiogenesis and Promotes Recovery After Myocardial Infarction.Journal of the American Heart Association · 2022Article
- Relevance of stromal interaction molecule 1 (STIM1) in experimental and human stroke.Pflugers Archiv : European journal of physiology · 2022Review
- Role of Store-Operated CaBiomolecules · 2021Review
- Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021Review
- SARAF and Orai1 Contribute to Endothelial Cell Activation and Angiogenesis.Frontiers in cell and developmental biology · 2021Article
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Salivary Cytokines and Airways Disease Severity in Patients with Cystic Fibrosis.Diagnostics (Basel, Switzerland) · 2020Article
- Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion.International journal of molecular sciences · 2020Review
- Endothelial CaInternational journal of molecular sciences · 2019Review
- Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling.Comprehensive Physiology · 2019Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In endothelial cells Ca(2+) entry is an essential component of the Ca(2+) signal that takes place during processes such as cell proliferation or angiogenesis. Ca(2+) influx occurs via the store-operated Ca(2+) entry pathway, involving stromal interaction molecule-1 (STIM1) and Orai1, but also through channels gated by second messengers like the transient receptor potential canonical (TRPC) channels. The human umbilical vein-derived endothelial cell line EA.hy926 expressed STIM1 and Orai1 as well as several TRPC channels. By invalidating each of these molecules, we showed that TRPC3, TRPC4, and TRPC5 are essential for the formation of tubular structures observed after EA.hy926 cells were plated on Matrigel. On the contrary, the silencing of STIM1 or Orai1 did not prevent tubulogenesis. Soon after being plated on Matrigel, the cells displayed spontaneous Ca(2+) oscillations that were strongly reduced by treatment with siRNA against TRPC3, TRPC4, or TRPC5, but not siRNA against STIM1 or Orai1. Furthermore, we showed that cell proliferation was reduced upon siRNA treatment against TRPC3, TRPC5, and Orai1 channels, whereas the knockdown of STIM1 had no effect. On primary human umbilical vein endothelial cells, TRPC1, TRPC4, and STIM1 are involved in tube formation, whereas Orai1 has no effect. These data showed that TRPC channels are essential for in vitro tubulogenesis, both on endothelial cell line and on primary endothelial cells.
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