Evidence map›Paper›PMID 24621388›Full record

ArticleJournal of cellular and molecular medicine2014

Period 2 is essential to maintain early endothelial progenitor cell function in vitro and angiogenesis after myocardial infarction in mice.

Yuan-Yuan Sun, Wen-Wu Bai, Bo Wang, Xiao-Ting Lu, Yi-Fan Xing, Wen Cheng, Xiao-Qiong Liu, Yu-Xia Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Clock gene Per2 modulates epidermal tissue repair in vivo.Journal of cellular biochemistry · 2024
    Article
  7. Article
  8. The Circadian Biology of Heart Failure.Circulation research · 2023
    Review
  9. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Circadian clock and the onset of cardiovascular events.Hypertension research : official journal of the Japanese Society of Hypertension · 2016
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Yuan-Yuan SunKey Laboratory of Cardiovascular Remodeling and Function Research, Qilu Hospital, Shandong University, Jinan, Shandong, China; Department of Traditional Chinese Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Wen-Wu Bai
Bo Wang
Xiao-Ting Lu
Yi-Fan Xing
Wen Cheng
Xiao-Qiong Liu
Yu-Xia Zhao
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular therapeutic neovascularization has been successfully performed in clinical trials for patients with ischaemia diseases. Despite the vast knowledge of cardiovascular disease and circadian biology, the role of the circadian clock in regulating angiogenesis in myocardial infarction (MI) remains poorly understood. In this study, we aimed to investigate the role and underlying mechanisms of Period 2 (Per2) in endothelial progenitor cell (EPC) function. Flow cytometry revealed lower circulating EPC proportion in per2(-/-) than in wild-type (WT) mice. PER2 was abundantly expressed in early EPCs in mice. In vitro, EPCs from per2(-/-) mice showed impaired proliferation, migration, tube formation and adhesion. Western blot analysis demonstrated inhibited PI3k/Akt/FoxO signalling and reduced C-X-C chemokine receptor type 4 (CXCR4) protein level in EPCs of per2(-/-) mice. The impaired proliferation was blocked by activated PI3K/Akt/FoxO signalling. Direct interaction of CXCR4 and PER2 was detected in WT EPCs. To further study the effect of per2 on in vivo EPC survival and angiogenesis, we injected saline or DiI-labelled WT or per2(-/-) EPC intramyocardially into mice with induced MI. Per2(-/-) reduced the retention of transplanted EPCs in the myocardium, which was associated with significantly reduced DiI expression in the myocardium of MI mice. Decreased angiogenesis in the myocardium of per2(-/-) EPC-treated mice coincided with decreased LV function and increased infarct size in the myocardium. Per2 may be a key factor in maintaining EPC function in vitro and in therapeutic angiogenesis in vivo.

Indexed as

Neovascularization, PhysiologicAnimalsApoptosisCell AdhesionCell CountCell MovementCell ProliferationCells, CulturedEndothelial Progenitor CellsForkhead Transcription FactorsHeart Function TestsMaleMice, Inbred C57BLMyocardial InfarctionPeriod Circadian ProteinsPhosphatidylinositol 3-KinasesForkhead Transcription FactorsPer2 protein, mousePeriod Circadian ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR4angiogenesisendothelial progenitor cellsmyocardial infarctionperiod 2

Identifiers

PMID24621388
PMCPMC4119396
OpenAlexW1975727657

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.