ArticlePloS one2014
Enhanced expression of Stim, Orai, and TRPC transcripts and proteins in endothelial progenitor cells isolated from patients with primary myelofibrosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 66 citations in OpenAlex.
- The CaInternational journal of molecular sciences · 2026Article
- The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.Frontiers in physiology · 2025Article
- Role of stretch-activated channels in light-generated action potentials mediated by an intramembrane molecular photoswitch.Journal of translational medicine · 2024Article
- Silencing of transient receptor potential canonical channel 4 inhibits endothelial progenitor cell angiogenesis by suppressing VEGF and SDF-1.American journal of translational research · 2024Article
- Cytological, molecular, cytogenetic, and physiological characterization of a novel immortalized human enteric glial cell line.Frontiers in cellular neuroscience · 2023Article
- INPP5A/HLA-G1/IL-10/MMP-21 Axis in Progression of Esophageal Squamous Cell CarcinomaIranian biomedical journal · 2022Article
- Store-Operated Calcium Channels Control Proliferation and Self-Renewal of Cancer Stem Cells from Glioblastoma.Cancers · 2021Article
- X-Ray Causes mRNA Transcripts Change to Enhance Orai2-Mediated CaFrontiers in molecular biosciences · 2021Article
- Type 2 Diabetes Alters Intracellular CaInternational journal of molecular sciences · 2019Article
- Pathophysiology of Calcium Mediated Ventricular Arrhythmias and Novel Therapeutic Options with Focus on Gene Therapy.International journal of molecular sciences · 2019Review
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- Familial Polyposis Coli: The Management of Desmoid Tumor Bleeding.Open medicine (Warsaw, Poland) · 2019Article
- Bradykinin-mediated CaJournal of cellular and molecular medicine · 2018Article
- Stim and Orai mediate constitutive CaOncotarget · 2018Article
- Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Endothelial CaInternational journal of molecular sciences · 2018Review
- Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated CaBioMed research international · 2018Article
- Polychlorinated biphenyl 19 blocks the most common form of store-operated CaNaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- VEGF-induced intracellular CaOncotarget · 2017Article
- Cell Based Therapeutic Approach in Vascular Surgery: Application and Review.Open medicine (Warsaw, Poland) · 2017Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAn increase in the frequency of circulating endothelial colony forming cells (ECFCs), the only subset of endothelial progenitor cells (EPCs) truly belonging to the endothelial phenotype, occurs in patients affected by primary myelofibrosis (PMF). Herein, they might contribute to the enhanced neovascularisation of fibrotic bone marrow and spleen. Store-operated Ca2+ entry (SOCE) activated by the depletion of the inositol-1,4,5-trisphosphate (InsP3)-sensitive Ca2+ store drives proliferation in ECFCs isolated from both healthy donors (N-ECFCs) and subjects suffering from renal cellular carcinoma (RCC-ECFCs). SOCE is up-regulated in RCC-ECFCs due to the over-expression of its underlying molecular components, namely Stim1, Orai1, and TRPC1. METHODOLOGY/PRINCIPAL
findingsWe utilized Ca2+ imaging, real-time polymerase chain reaction, western blot analysis and functional assays to evaluate molecular structure and the functional role of SOCE in ECFCs derived from PMF patients (PMF-ECFCs). SOCE, induced by either pharmacological (i.e. cyclopiazonic acid or CPA) or physiological (i.e. ATP) stimulation, was significantly higher in PMF-ECFCs. ATP-induced SOCE was inhibited upon blockade of the phospholipase C/InsP3 signalling pathway with U73111 and 2-APB. The higher amplitude of SOCE was associated to the over-expression of the transcripts encoding for Stim2, Orai2-3, and TRPC1. Conversely, immunoblotting revealed that Stim2 levels remained constant as compared to N-ECFCs, while Stim1, Orai1, Orai3, TRPC1 and TRPC4 proteins were over-expressed in PMF-ECFCs. ATP-induced SOCE was inhibited by BTP-2 and low micromolar La3+ and Gd3+, while CPA-elicited SOCE was insensitive to Gd3+. Finally, BTP-2 and La3+ weakly blocked PMF-ECFC proliferation, while Gd3+ was ineffective.
conclusionsTwo distinct signalling pathways mediate SOCE in PMF-ECFCs; one is activated by passive store depletion and is Gd3+-resistant, while the other one is regulated by the InsP3-sensitive Ca2+ pool and is inhibited by Gd3+. Unlike N- and RCC-ECFCs, the InsP3-dependent SOCE does not drive PMF-ECFC proliferation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.