Evidence map›Paper›PMID 27231894›Full record

ArticleInternational journal of molecular sciences2016

Cardiac Stem Cell Secretome Protects Cardiomyocytes from Hypoxic Injury Partly via Monocyte Chemotactic Protein-1-Dependent Mechanism.

Chi-Yeon Park, Seung-Cheol Choi, Jong-Ho Kim, Ji-Hyun Choi, Hyung Joon Joo, Soon Jun Hong, Do-Sun Lim

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Development of aInternational journal of molecular sciences · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Secretome Analysis Performed DuringFrontiers in cell and developmental biology · 2020
    Article
  12. 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

7 authors.

Chi-Yeon ParkDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. chiyoun@korea.ac.kr.
Seung-Cheol ChoiDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. choisc86@gmail.com.
Jong-Ho KimDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. mecey@naver.com.
Ji-Hyun ChoiDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. j2610@hanmail.net.
Hyung Joon JooDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. drjoohj@gmail.com.
Soon Jun HongDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. psyche94@gmail.com.
Do-Sun LimDepartment of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul 02841, Korea. dslmd@kumc.or.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac stem cells (CSCs) were known to secrete diverse paracrine factors leading to functional improvement and beneficial left ventricular remodeling via activation of the endogenous pro-survival signaling pathway. However, little is known about the paracrine factors secreted by CSCs and their roles in cardiomyocyte survival during hypoxic condition mimicking the post-myocardial infarction environment. We established Sca-1+/CD31- human telomerase reverse transcriptase-immortalized CSCs (Sca-1+/CD31- CSCs(hTERT)), evaluated their stem cell properties, and paracrine potential in cardiomyocyte survival during hypoxia-induced injury. Sca-1+/CD31- CSCs(hTERT) sustained proliferation ability even after long-term culture exceeding 100 population doublings, and represented multi-differentiation potential into cardiomyogenic, endothelial, adipogenic, and osteogenic lineages. Dominant factors secreted from Sca-1+/CD31- CSCs(hTERT) were EGF, TGF-β1, IGF-1, IGF-2, MCP-1, HGF R, and IL-6. Among these, MCP-1 was the most predominant factor in Sca-1+/CD31- CSCs(hTERT) conditioned medium (CM). Sca-1+/CD31- CSCs(hTERT) CM increased survival and reduced apoptosis of HL-1 cardiomyocytes during hypoxic injury. MCP-1 silencing in Sca-1+/CD31- CSCs(hTERT) CM resulted in a significant reduction in cardiomyocyte apoptosis. We demonstrated that Sca-1+/CD31- CSCs(hTERT) exhibited long-term proliferation capacity and multi-differentiation potential. Sca-1+/CD31- CSCs(hTERT) CM protected cardiomyocytes from hypoxic injury partly via MCP-1-dependent mechanism. Thus, they are valuable sources for in vitro and in vivo studies in the cardiovascular field.

Indexed as

AnimalsCell DifferentiationCell HypoxiaCell ProliferationCells, CulturedCell SurvivalChemokine CCL2HumansMiceModels, BiologicalMyocytes, CardiacPlatelet Endothelial Cell Adhesion Molecule-1Stem CellsTelomeraseCcl2 protein, mouseChemokine CCL2Platelet Endothelial Cell Adhesion Molecule-1TelomeraseTERT protein, humancardiac stem cellscardiomyocyte survivalimmortalizationMCP-1secretome

Identifiers

PMID27231894
PMCPMC4926334

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.