ArticleStem cells and development2012
Knockdown of transient receptor potential canonical-1 reduces the proliferation and migration of endothelial progenitor cells.
Article in Stem cells and development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 61 citations in OpenAlex.
- Cognitive-Enhancing Effects of Bioactive Compounds and Traditional Herbal Medicines in Elderly Patients with Metabolic Syndrome.Biomolecules · 2026Review
- Transient receptor potential canonical 3/5 attenuate endothelial damage-induced neointima formation without affecting endothelial cell proliferation.European journal of histochemistry : EJH · 2025Article
- CaBiomolecules · 2023Article
- New Insights into TRP Ion Channels in Stem Cells.International journal of molecular sciences · 2022Review
- Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022Review
- Mechanosensitive ion channels in cell migration.Cells & development · 2021Review
- Transient Receptor Potential (TRP) Channels in Haematological Malignancies: An Update.Biomolecules · 2021Review
- Effects and mechanisms of basic fibroblast growth factor on the proliferation and regenerative profiles of cryopreserved dental pulp stem cells.Cell proliferation · 2021Article
- Impact of Na+ permeation on collective migration of pulmonary arterial endothelial cells.PloS one · 2021Article
- Review
- 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
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- TRPC1 intensifies house dust mite-induced airway remodeling by facilitating epithelial-to-mesenchymal transition and STAT3/NF-κB signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- TRPC1 Deficiency Impairs the Endothelial Progenitor Cell Function via Inhibition of Calmodulin/eNOS Pathway.Journal of cardiovascular translational research · 2018Article
- Article
- Activation of Transient Receptor Potential Vanilloid 4 Promotes the Proliferation of Stem Cells in the Adult Hippocampal Dentate Gyrus.Molecular neurobiology · 2017Article
- ATP-induced CaCellular and molecular life sciences : CMLS · 2017Review
- TRPC1- and TRPC3-dependent CaGlia · 2017Article
- Crosstalk between calcium and reactive oxygen species signaling in cancer.Cell calcium · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial progenitor cells (EPCs) play an important role in accelerating endothelial repair after vascular injury. The proliferation and migration of EPCs is a critical first step in restoring endothelial. However, mechanisms for modulating EPC proliferation and migration are still being elucidated. Our previous study found that transient receptor potential canonical-1 (TRPC1) is involved in regulating store-operated Ca(2+) entry in EPCs through stromal interaction molecule 1. Therefore, in the present study, we sought to further investigate the regulation of proliferation and migration of EPCs by TRPC1. We found that the silencing of TRPC1 by 2 different RNA interference methods suppressed the proliferation and migration of EPCs. In addition, knockdown of TRPC1 significantly reduced of the amplitude of store-operated Ca(2+) entry and caused arrest of the EPC cell cycle in G1 phase. Analysis of the expression of 84 cell cycle genes by microarray showed that 9 genes were upregulated and 4 were downregulated by >2-fold in EPCs following TRPC1 silencing. The genes with expression changes were Ak1, Brca2, Camk2b, p21, Ddit3, Inha, Slfn1, Mdm2, Prm1, Bcl2, Mki67, Pmp22, and Ppp2r3a. Finally, we found that a Schlafen 1-blocking peptide partially reversed the abnormal cell cycle distribution and proliferation induced by TRPC1 knockdown, suggesting that Schlafen 1 is downstream of TRPC1 silencing in regulating EPC proliferation. In summary, these findings provide a new mechanism for modulating the biological properties of EPCs and suggest that TRPC1 may be a new target for inducing vascular repair by EPCs.
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Registered trials
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.