Evidence map›Paper›PMID 25888601›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015

Mesenchymal stem cell-derived inflammatory fibroblasts promote monocyte transition into myeloid fibroblasts via an IL-6-dependent mechanism in the aging mouse heart.

Katarzyna A Cieslik, JoAnn Trial, Mark L Entman

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  9. Article
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  12. IL-18/IL-18R1 promotes circulating fibrocyte differentiation in the aging population.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  18. Article
  19. The influence of diet on anti-cancer immune responsiveness.Journal of translational medicine · 2018
    Review
  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

3 authors at 1 institution in 1 country.

Katarzyna A CieslikDivision of Cardiovascular Sciences and the DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA cieslik@bcm.edu.
JoAnn TrialDivision of Cardiovascular Sciences and the DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Mark L EntmanDivision of Cardiovascular Sciences and the DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Baylor College of Medicine · US

Funding

Role of Blood-Borne Fibroblast Precursors in Ischemic CardiomyopathyR01HL089792 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ENTMAN, MARK L · 2007 to 2016
$3.4M
NHLBI NIH HHS R01 HL089792NHLBI NIH HHS R01HL089792
6 · The paper itself

Abstract

Fibrosis in the old mouse heart arises partly as a result of aberrant mesenchymal fibroblast activation. We have previously shown that endogenous mesenchymal stem cells (MSCs) in the aged heart are markedly resistant to TGF-β signaling. Fibroblasts originating from these MSCs retain their TGF-β unresponsiveness and become inflammatory. In current studies, we found that these inflammatory fibroblasts secreted higher levels of IL-6 (3-fold increase, P < 0.05) when compared with fibroblasts derived from the young hearts. Elevated IL-6 levels in fibroblasts derived from old hearts arose from up-regulated expression of Ras protein-specific guanine nucleotide releasing factor 1 (RasGrf1), a Ras activator (5-fold, P < 0.01). Knockdown of RasGrf1 by gene silencing or pharmacologic inhibition of farnesyltransferase (FTase) or ERK caused reduction of IL-6 mRNA (more than 65%, P < 0.01) and decreased levels of secreted IL-6 (by 44%, P < 0.01). In vitro, IL-6 markedly increased monocyte chemoattractant protein-1-driven monocyte-to-myeloid fibroblast formation after transendothelial migration (TEM; 3-fold, P < 0.01). In conclusion, abnormal expression of RasGrf1 promoted production of IL-6 by mesenchymal fibroblasts in the old heart. Secreted IL-6 supported conversion of monocyte into myeloid fibroblasts. This process promotes fibrosis and contributes to the diastolic dysfunction in the aging heart.

Indexed as

AgingAnimalsCells, CulturedFibroblastsFibrosisHeartInflammationInterleukin-6MaleMesenchymal Stem CellsMiceMice, Inbred C57BLMonocytesMyeloid CellsTransforming Growth Factor betaInterleukin-6interleukin-6, mouseTransforming Growth Factor betafibrosisRasGrf1transendothelial migration

Identifiers

PMID25888601
PMCPMC4511196
OpenAlexW2032677697

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.