ArticlePloS one2014
Nucleolin down-regulation is involved in ADP-induced cell cycle arrest in S phase and cell apoptosis in vascular endothelial cells.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
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- Adenosine diphosphate stimulates VEGF-independent choroidal endothelial cell proliferation: A potential escape from anti-VEGF therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ticagrelor Induces Angiogenesis in Progenitor and Mature Endothelial Cells In Vitro: Investigation of the Possible Role of Adenosine.International journal of molecular sciences · 2024Article
- Longitudinal shear stress response in human endothelial cells to atheroprone and atheroprotective conditions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cancer Stem Cells and Nucleolin as Drivers of Carcinogenesis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Triptolide interrupts rRNA synthesis and induces the RPL23‑MDM2‑p53 pathway to repress lung cancer cells.Oncology reports · 2020Article
- Effect of nucleolin on adriamycin resistance via the regulation of B-cell lymphoma 2 expression in Burkitt's lymphoma cells.Journal of cellular physiology · 2019Article
- Ticagrelor suppresses oxidized low‑density lipoprotein‑induced endothelial cell apoptosis and alleviates atherosclerosis in ApoE‑/‑ mice via downregulation of PCSK9.Molecular medicine reports · 2019Article
- Epigenetic mediated zinc finger protein 671 downregulation promotes cell proliferation and tumorigenicity in nasopharyngeal carcinoma by inhibiting cell cycle arrest.Journal of experimental & clinical cancer research : CR · 2017Article
- P2YJournal of pain research · 2017Article
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7 authors at 1 institution in 1 country.
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Abstract
High concentration of extracellular ADP has been reported to induce cell apoptosis, but the molecular mechanisms remain not fully elucidated. In this study, we found by serendipity that ADP treatment of human umbilical vein endothelial cells (HUVEC) and human aortic endothelial cells (HAEC) down-regulated the protein level of nucleolin in a dose- and time-dependent manner. ADP treatment did not decrease the transcript level of nucloelin, suggesting that ADP might induce nucleolin protein degradation. HUVEC and HAEC expressed ADP receptor P2Y13 receptor, but did not express P2Y1 or P2Y12 receptors. However, P2Y1, 12, 13 receptor antagonists MRS2179, PSB0739, MRS2211 did not inhibit ADP-induced down-regulation of nucleolin. Moreover, MRS2211 itself down-regulated nucleolin protein level. In addition, 2-MeSADP, an agonist for P2Y1, 12 and 13 receptors, did not down-regulate nucleolin protein. These results suggested that ADP-induced nucleolin down-regulation was not due to the activation of P2Y1, 12, or 13 receptors. We also found that ADP treatment induced cell cycle arrest in S phase, cell apoptosis and cell proliferation inhibition via nucleolin down-regulation. The over-expression of nucleolin by gene transfer partly reversed ADP-induced cell cycle arrest, cell apoptosis and cell proliferation inhibition. Furthermore, ADP sensitized HUVEC to cisplatin-induced cell death by the down-regulation of Bcl-2 expression. Taken together, we found, for the first time to our knowledge, a novel mechanism by which ADP regulates cell proliferation by induction of cell cycle arrest and cell apoptosis via targeting nucelolin.
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