Evidence map›Paper›PMID 24891120›Full record

ArticleBiotechnology and bioengineering2014

Fractional factorial design to investigate stromal cell regulation of macrophage plasticity.

Jeffrey A Barminko, Nir I Nativ, Rene Schloss, Martin L Yarmush

Abstract read
In one paragraph

Article in Biotechnology and bioengineering, 2014. 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
4.1field-weighted citation impact, top 6% 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, 34 citations in OpenAlex.

  1. Review
  2. Osteoarthritis and cartilage open · 2024
    Article
  3. Article
  4. Article
  5. Macrophages as a therapeutic target to promote diabetic wound healing.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  6. Review
  7. Review
  8. Review
  9. Innate immune cell-epithelial crosstalk during wound repair.The Journal of clinical investigation · 2019
    Review
  10. Article
  11. Tissue-Engineered Heart Valves: A Call for Mechanistic Studies.Tissue engineering. Part B, Reviews · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Prostaglandin ENano LIFE · 2017
    Article
  16. Article
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Jeffrey A BarminkoDepartment of Biomedical Engineering, Rutgers, The State University of New Jersey, 599 Taylor Road, Piscataway, New Jersey, 08854.
Nir I Nativ
Rene Schloss
Martin L Yarmush
Rutgers, The State University of New Jersey · US

Funding

UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
Lumbar Puncture Delivery of MSC & Function in Spinal Cord InjuryR21NS070175 · NINDS · RUTGERS, THE STATE UNIV OF N.J. · PI GRUMET, MARTIN H · 2010 to 2011
$420k
NIGMS NIH HHS T32 GM008339NIGMS NIH HHS T32 GM00833923NINDS NIH HHS NS070175NINDS NIH HHS R21 NS070175
6 · The paper itself

Abstract

Understanding the regulatory networks which control specific macrophage phenotypes is essential in identifying novel targets to correct macrophage mediated clinical disorders, often accompanied by inflammatory events. Since mesenchymal stromal cells (MSCs) have been shown to play key roles in regulating immune functions predominantly via a large number of secreted products, we used a fractional factorial approach to streamline experimental evaluation of MSC mediated inflammatory macrophage regulation. Our macrophage reprogramming metrics, human bone marrow MSC attenuation of macrophage pro-inflammatory M1 TNFα secretion and simultaneous enhanced expression of the M2 macrophage marker, CD206, were used as analysis endpoints. Objective evaluation of a panel of MSC secreted mediators indicated that PGE2 alone was sufficient in facilitating macrophage reprogramming, while IL4 only provided partial reprogramming. Inhibiting stromal cell PGE2 secretion with Indomethacin, reversed the macrophage reprogramming effect. PGE2 reprogramming was mediated through the EP4 receptor and indirectly through the CREB signaling pathway as GSK3 specific inhibitors induced M1 macrophages to express CD206. This reprogramming pathway functioned independently from the M1 suppression pathway, as neither CREB nor GSK3 inhibition reversed PGE2 TNF-α secretion attenuation. In conclusion, fractional factorial experimental design identified stromal derived PGE2 as the factor most important in facilitating macrophage reprogramming, albeit via two unique pathways.

Indexed as

DinoprostoneHumansInterleukin-4Lectins, C-TypeMacrophagesMannose-Binding LectinsMannose ReceptorMesenchymal Stem CellsPhenotypeReceptors, Cell SurfaceTumor Necrosis Factor-alphaDinoprostoneIL4 protein, humanInterleukin-4Lectins, C-TypeMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceTumor Necrosis Factor-alphafractional factorial designmacrophagemesenchymal stromal cellsPGE2

Identifiers

PMID24891120
PMCPMC5928506
OpenAlexW2144172086

What OpenQuestion holds

Textmetadata
LicenceTDM
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.