Evidence map›Paper›PMID 28138512›Full record

ArticleRegenerative engineering and translational medicine2016

Aging Affects Bone Marrow Macrophage Polarization: Relevance to Bone Healing.

E Gibon, F Loi, Luis A Córdova, J Pajarinen, T Lin, L Lu, A Nabeshima, Z Yao, Stuart B Goodman

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Regenerative engineering and translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Consequences of Aging on Bone.Aging and disease · 2023
    Pooled it
  2. Article
  3. Review
  4. Article
  5. p21Nature aging · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

E GibonDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA; Laboratoire de Biomécanique et Biomatériaux Ostéo-Articulaires -UMR CNRS 7052, Faculté de Médecine - Université Paris7, 10 avenue de Verdun, 75010 Paris, France; Department of Orthopaedic Surgery, Hopital Cochin, APHP, Université Paris5, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France.
F LoiDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
Luis A CórdovaDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA; Department of Oral and Maxillofacial Surgery, University of Chile-Conicyt, Santiago, Chile.
J PajarinenDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
T LinDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
L LuDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
A NabeshimaDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
Z YaoDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA.
Stuart B GoodmanDepartment of Orthopaedic Surgery, Stanford University, R116, 300 Pasteur Drive, Stanford, CA 94305, USA; Department of Bioengineering, Stanford University, Stanford, CA, USA; Department of Orthopaedic Surgery and (by courtesy) Bioengineering, Stanford University Medical Center Outpatient Center, 450 Broadway St., M/C 6342, Redwood City, CA 94063, USA.
Stanford University · US

Funding

Wear Particle Disease and NF-kappa B SignalingR01AR063717 · NIAMS · STANFORD UNIVERSITY · PI GOODMAN, STUART B · 2012 to 2021
$3.5M
Chemokine Directed Cell Trafficking during Continuous Infusion of Wear ParticlesR01AR055650 · NIAMS · STANFORD UNIVERSITY · PI GOODMAN, STUART B · 2007 to 2016
$3.3M
NIAMS NIH HHS R01 AR055650NIAMS NIH HHS R01 AR063717
6 · The paper itself

Abstract

Macrophages are an important component of the inflammatory cascade by initiating and modulating the processes leading to tissue regeneration and bone healing. Depending on the local environment, macrophages can be polarized into M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes. In order to assess the effects of aging on macrophage function, bone marrow macrophage polarization using primary bone marrow macrophages (BMMs) from young (8 weeks old) and aged (72 weeks old) wild-type male C57BL/6J mice was analyzed. Fluorescence-activated cell sorting (FACS) analysis (CD11b, iNOS, CD206), qRT-PCR (iNOS, TNF-α, CD206, Arginase 1), and ELISA (TNF-α, IL-1ra) were performed to compare the M1 and M2 phenotypic markers in young and aged mouse macrophages. Once M1 and M2 macrophage phenotypes were confirmed, the results showed that TNF-α mRNA was significantly upregulated in aged M1s after interferon gamma (INF-γ) exposure. Arginase 1 and CD206 mRNA expression were still upregulated with IL4 stimulation in aged macrophages, but to a lesser extend than those from younger animals. TNF-α secretion was also significantly increased in aged M1s compared to young M1s, following lipopolysaccharide (LPS) exposure. However, the IL-1ra secretion did not increase accordingly in aged mice. The results demonstrate that, compared to younger animals, aging of bone marrow derived macrophages increases the resting levels of oxidative stress, and the ratios of pro- to anti-inflammatory markers. These age-related changes in macrophage polarization may explain in part the attenuated response to adverse stimuli and delay in processes such as fracture healing seen in the elderly. LAY SUMMARY: Bone healing is a complex process that involves both biological and mechanical factors. Macrophages are key cells that regulate the events involved in bone healing, especially the initial inflammatory phase. In this biological cascade of events, macrophages present as different functional phenotypes including uncommitted (M0), pro-inflammatory (M1), and anti-inflammatory (M2), a process called macrophage polarization. A clear understanding of the effects of aging on macrophage polarization is critical to modulating adverse events such as fractures, atraumatic bone loss, and tissue regeneration in an aging population.

Indexed as

AgingBone healingBone marrowmacrophagePolarization

Identifiers

PMID28138512
PMCPMC5270653
OpenAlexW2435513334

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.