Evidence map›Paper›PMID 27490266›Full record

ArticleAging2016

Paracrine effects of human adipose-derived mesenchymal stem cells in inflammatory stress-induced senescence features of osteoarthritic chondrocytes.

Julia Platas, Maria Isabel Guillén, Maria Dolores Pérez Del Caz, Francisco Gomar, Miguel Angel Castejón, Vicente Mirabet, Maria José Alcaraz

Open access · greenAbstract read
In one paragraph

Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  13. Review
  14. Ferroptosis in Osteoarthritis: Current Understanding.Journal of inflammation research · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Mesenchymal Stem Cells and Their Exocytotic Vesicles.International journal of molecular sciences · 2023
    Review
  20. Extracellular Vesicles and Cardiac Aging.Advances in experimental medicine and biology · 2023
    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 at 4 institutions in 1 country.

Julia PlatasDepartment of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain.
Maria Isabel GuillénDepartment of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain.
Maria Dolores Pérez Del CazDepartment of Burn and Plastic Surgery, La Fe Polytechnic University Hospital, 46026 Valencia, Spain.
Francisco GomarDepartment of Surgery, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain.
Miguel Angel CastejónDepartment of Orthopaedic Surgery and Traumatology, De la Ribera University Hospital, Alzira, 46600 Valencia, Spain.
Vicente MirabetValencia Transfusion Center, Generalitat Valenciana, 46014 Valencia, Spain.
Maria José AlcarazDepartment of Pharmacology and IDM, University of Valencia, Burjasot, 46100 Valencia, Spain.
Universitat de València · ESGeneralitat Valenciana · ESHospital de La Ribera · ESHospital Universitari i Politècnic La Fe · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging and exposure to stress would determine the chondrocyte phenotype in osteoarthritis (OA). In particular, chronic inflammation may contribute to stress-induced senescence of chondrocytes and cartilage degeneration during OA progression. Recent studies have shown that adipose-derived mesenchymal stem cells exert paracrine effects protecting against degenerative changes in chondrocytes. We have investigated whether the conditioned medium (CM) from adipose-derived mesenchymal stem cells may regulate senescence features induced by inflammatory stress in OA chondrocytes. Our results indicate that CM down-regulated senescence markers induced by interleukin-1β including senescence-associated β-galactosidase activity, accumulation of γH2AX foci and morphological changes with enhanced formation of actin stress fibers. Treatment of chondrocytes with CM also decreased the production of oxidative stress, the activation of mitogen-activated protein kinases, and the expression of caveolin-1 and p21. The effects of CM were related to the reduction in p53 acetylation which would be dependent on the enhancement of Sirtuin 1 expression. Therefore, CM may exert protective effects in degenerative joint conditions by countering the premature senescence of OA chondrocytes induced by inflammatory stress.

Indexed as

Adipose Tissuebeta-GalactosidaseCaveolin 1Cellular SenescenceChondrocytesHumansInflammationMesenchymal Stem CellsOsteoarthritisOxidative StressParacrine Communicationbeta-GalactosidaseCAV1 protein, humanCaveolin 1adipose-derived mesenchymal stem cells conditioned mediumchondrocytesinflammationsenescence

Identifiers

PMID27490266
PMCPMC5032691
OpenAlexW2503305289

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.