ArticleBritish journal of pharmacology2012
Adenosine-5'-triphosphate up-regulates proliferation of human cardiac fibroblasts.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Shock wave treatment enhances cell proliferation and improves wound healing by ATP release-coupled extracellular signal-regulated kinase (ERK) activation.The Journal of biological chemistry · 2014Trial
- Probenecid-Mediated Pannexin-1 Inhibition Preserves βFGF-Driven Regenerative Responses in Human Dermal Fibroblasts.International journal of molecular sciences · 2026Article
- CaBiomedicines · 2025Review
- CaBiomolecules · 2024Review
- Impact of Interdependent CaCell biochemistry and biophysics · 2023Article
- The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023Article
- Yes-Associated Protein (Yap) Is Up-Regulated in Heart Failure and Promotes Cardiac Fibroblast Proliferation.International journal of molecular sciences · 2021Article
- P2Y1 Receptor Agonist Attenuates Cardiac Fibroblasts Activation Triggered by TGF-β1.Frontiers in pharmacology · 2021Article
- Resolving the Ionotropic P2X4 Receptor Mystery Points Towards a New Therapeutic Target for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- CaJournal of cardiovascular development and disease · 2019Review
- Protective transcriptional mechanisms in cardiomyocytes and cardiac fibroblasts.Journal of molecular and cellular cardiology · 2019Review
- HIF-1α contributes to tube malformation of human lymphatic endothelial cells by upregulating VEGFR-3.International journal of oncology · 2019Article
- Endostatin Stimulates Proliferation and Migration of Myofibroblasts Isolated from Myocardial Infarction Model Rats.International journal of molecular sciences · 2018Article
- N6-(2-Hydroxyethyl) Adenosine FromFrontiers in physiology · 2018Article
- Acute rejection after kidney transplantation promotes graft fibrosis with elevated adenosine level in rat.PloS one · 2017Article
- Functional TRPV2 and TRPV4 channels in human cardiac c-kit(+) progenitor cells.Journal of cellular and molecular medicine · 2016Article
- Inferring Growth Control Mechanisms in Growing Multi-cellular Spheroids of NSCLC Cells from Spatial-Temporal Image Data.PLoS computational biology · 2016Article
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Effects of BKCa and Kir2.1 Channels on Cell Cycling Progression and Migration in Human Cardiac c-kit+ Progenitor Cells.PloS one · 2015Article
- P2Y2 purinergic receptor activation is essential for efficient hepatocyte proliferation in response to partial hepatectomy.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeATP is a potent signalling molecule that regulates biological activities including increasing or decreasing proliferation in different types of cells. The aim of the present study was to investigate how ATP regulates the proliferation of human cardiac fibroblasts. EXPERIMENTAL APPROACH: Reverse transcription (RT)-PCR, Western blot analysis, cell proliferation and migration assays were employed to investigate the effects of ATP on human adult ventricular fibroblasts. KEY
resultsATP increased cell proliferation in a concentration-dependent manner. Similarly, the P2X receptor agonist α,β-methylene ATP and P2Y receptor agonist ATP-γS also up-regulated cell proliferation. The P2 receptor antagonists suramin and reactive blue-2 prevented the ATP-induced increase in proliferation and RT-PCR and Western blot analysis revealed that mRNAs of P2X(4/7) and P2Y(2) are abundant in cardiac fibroblasts. ATP increased phosphorylated PKB (Akt) and ERK1/2 levels; an effect antagonized by suramin, reactive blue-2, the PI3-kinase inhibitor, wortmannin, PKB inhibitor, API-2, and MAPK inhibitor, PD98059. These kinase inhibitors also prevented the ATP-induced increase in proliferation. In addition, ATP enhanced the progression of cells from the G0/G1 phase to the S phase by increasing the expression of proteins for cyclin D1 and cyclin E. Silencing the P2X(4/7) and P2Y(2) receptors with siRNA targeting the corresponding receptor diminished ATP-stimulated proliferation and migration of the cardiac fibroblasts. CONCLUSION AND IMPLICATION: ATP activates P2X(4/7) and P2Y(2) receptors and up-regulates the proliferation of human cardiac fibroblasts by promoting cell cycling progression. It also increases the migration of these cells. These effects of ATP may be involved in cardiac remodelling of injured hearts.
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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.