ArticleStem cells and development2015
Reduction of Store-Operated Ca(2+) Entry Correlates with Endothelial Progenitor Cell Dysfunction in Atherosclerotic Mice.
Article in Stem cells and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 25 citations in OpenAlex.
- Research progress on the role and mechanism of STIM and Orai protein-mediated store-operated calcium entry in cardiovascular diseases.Channels (Austin, Tex.) · 2026Review
- Molecular Mechanisms Underlying Vascular Remodeling in Hypertension.Reviews in cardiovascular medicine · 2024Review
- Age-associated declined function of endothelial progenitor cells and its correlation with plasma IL-18 or IL-23 concentrations in patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2024Article
- cGAS-STING Pathway Performance in the Vulnerable Atherosclerotic Plaque.Aging and disease · 2022Article
- Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022Review
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Endothelial CaInternational journal of molecular sciences · 2019Review
- ORAI channels in cellular remodeling of cardiorespiratory disease.Cell calcium · 2019Review
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- Common Injuries and Repair Mechanisms in the Endothelial Lining.Chinese medical journal · 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
- ATP-induced CaCellular and molecular life sciences : CMLS · 2017Review
- Store-operated calcium entry-activated autophagy protects EPC proliferation via the CAMKK2-MTOR pathway in ox-LDL exposure.Autophagy · 2017Article
- miR-185 silencing promotes the progression of atherosclerosis via targeting stromal interaction molecule 1.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dysfunction of endothelial progenitor cells (EPCs) has been shown to prevent endothelial repair during the development of atherosclerosis (AS). Previous studies have revealed that store-operated calcium entry (SOCE) is an important factor in regulating EPC functions. However, whether this is also the mechanism in AS has not been elucidated. Therefore, we evaluated the role of SOCE in EPCs isolated from an atherosclerotic mouse model. Atheromatous plaques were more frequent in the aortas of ApoE(-/-) mice fed a high-fat diet for 16 weeks compared with controls, and the proliferative and migratory activities of atherosclerotic EPCs were significantly decreased. Accordingly, SOCE amplitude, as well as spontaneous or VEGF-induced Ca(2+) oscillations, decreased in atherosclerotic EPCs. These results may be associated with the downregulated expression of Stim1, Orai1, and TRPC1, which are major mediators of SOCE. In addition, eNOS expression and phosphorylation at Ser(1177), which are critical regulators of EPC function, were markedly reduced in the atherosclerotic EPCs. The impairment of eNOS activity could also be induced by using an SOCE inhibitor or by Stim1 gene silencing, indicating a link between the activities of eNOS and SOCE in AS. Furthermore, decreased SOCE function inhibited EPC proliferation and migration in vitro. In conclusion, our results showed that the reduction of SOCE induced EPC dysfunction during AS, potentially through downregulation of store-operated calcium channel (SOCC) components and impaired eNOS activity. Approaches aimed at reestablishing SOCE activity may thus improve the function of EPCs during AS.
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