Evidence map›Paper›PMID 19507001›Full record

ArticleMolecular and cellular biochemistry2009

The effects of mesenchymal stem cells on c-kit up-regulation and cell-cycle re-entry of neonatal cardiomyocytes are mediated by activation of insulin-like growth factor 1 receptor.

Xi-Yong Yu, Yong-Jian Geng, Xiao-Hong Li, Qiu-Xiong Lin, Zhi-Xin Shan, Shu-Guang Lin, Yao-Hua Song, Yangxin Li

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Application of stem cells in orthopedics.Stem cells international · 2012
    Article
  9. Review
  10. Review
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 4 institutions in 2 countries.

Xi-Yong YuMedical Research Center of Guangdong General Hospital, Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, 510080, People's Republic of China. yuxycn@hotmail.com
Yong-Jian Geng
Xiao-Hong Li
Qiu-Xiong Lin
Zhi-Xin Shan
Shu-Guang Lin
Yao-Hua Song
Yangxin Li
Guangdong Academy of Medical Sciences · CNGuangdong General Hospital · CNThe University of Texas Health Science Center at San Antonio · USThe University of Texas MD Anderson Cancer Center · US

Funding

CD1-RESTRICTED T CELL RESPONSE IN ATHEROSCLEROSISR01HL069509 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI GENG, YONG-JIAN · 2001 to 2004
$1.6M
NHLBI NIH HHS R01HL69509
6 · The paper itself

Abstract

C-kit-positive neonatal cardiomyocytes (NCMs) contribute to myocardial regeneration. However, the myocardium itself cannot give rise to a robust regenerative response owing to the limited numbers of c-kit-positive resident stem cells present in the heart. It has been shown that mesenchymal stem cells (MSCs) can enhance cardiac repair via the release of paracrine factors such as insulin-like growth factor (IGF-1). We investigated whether the increased expression of c-kit in NCMs mediates the beneficial effects of MSCs on cardiac repair. MSCs and NCMs were prepared from Lewis rats and co-cultured in a Transwell system, which allowed the diffusion of secreted factors but prevented cell contact between the two cell types. The proliferation of NCMs was determined by BrdU assay. The expression of c-kit was assessed by real-time PCR and flow cytometry. The apoptosis rate of NCMs in response to hypoxia was determined by flow cytometry. We found that the expression of c-kit in NCMs was increased by paracrine factors released by MSCs. The effect of paracrine factors on c-kit expression was attenuated by IGF-1 receptor-neutralizing antibody. Furthermore, we found that increased c-kit expression requires IGF-1 receptor activation via the phosphatidylinositol 3 kinase/Akt-mediated pathway. These findings provide a new paradigm for the biological effects of IGF-1 and have significant implications for understanding the beneficial effects of MSCs on myocardial regeneration.

Indexed as

Cell CycleAnimalsAnimals, NewbornAntibodies, NeutralizingApoptosisBlotting, WesternBone MarrowCell ProliferationCells, CulturedEnzyme-Linked Immunosorbent AssayFlow CytometryInsulin-Like Growth Factor IMesenchymal Stem CellsMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntibodies, NeutralizingInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-kitReceptor, IGF Type 1RNA, Messenger

Identifiers

PMID19507001
OpenAlexW2093936966

What OpenQuestion holds

Textmetadata
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.