ArticlePloS one2014
Period2 deficiency blunts hypoxia-induced mobilization and function of endothelial progenitor cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Circadian rhythm and the molecular clock in endothelial function of the cardiovascular system.Molecular and cellular biochemistry · 2026Review
- Research progress of circadian rhythm in cardiovascular disease: A bibliometric study from 2002 to 2022.Heliyon · 2024Review
- Circadian Effects on Vascular Immunopathologies.Circulation research · 2024Review
- Methamphetamine-induced changes in myocardial gene transcription are sex-dependent.BMC genomics · 2021Article
- Opportunities and challenges: stem cell-based therapy for the treatment of ischemic stroke.CNS neuroscience & therapeutics · 2015Review
- Correction: Period2 deficiency blunts hypoxia-induced mobilization and function of endothelial progenitor cells.PloS one · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the clinic, variations in circadian rhythm are evident in patients with cardiovascular disease, and the risk of cardiovascular events increases when rhythms are disrupted. In this study, we focused on the role of the circadian gene period2 (per2) in mobilization and function of endothelial progenitor cells (EPCs) in vitro and in vivo after myocardial infarction (MI) in mice. METHODS AND
resultsMI was produced by surgical ligation of the left anterior descending coronary artery in mice with and without per2 deficiency. Trans-thoracic echocardiography was used to evaluate cardiac function in mice. Per2-/- mice with MI showed decreased cardiac function and increased infarct size. The number of CD34+ cells and capillary density were decreased in the myocardium of per2-/- mice on immunohistochemistry. Flow cytometry revealed decreased number of circulating EPCs in per2-/- mice after MI. In vitro, per2-/- EPCs showed decreased migration and tube formation capacity under hypoxia. Western blot analysis revealed inhibited activation of extracellular signal-regulated kinase and Akt signaling in the bone marrow of per2-/- mice and inhibited PI3K/Akt expression in per2-/- EPCs under hypoxia.
conclusionsPer2 modulates EPC mobilization and function after MI, which is important to recovery after MI in mice.
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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.