Evidence map›Paper›PMID 39978574›Full record

ArticleOsteoarthritis and cartilage2025

Macrophage phenotypes modulate neoangiogenesis and fibroblast profiles in synovial-like organoid cultures.

Qi Gao, Xiurui Zhang, Meagan J Makarcyzk, Laurel Elizabeth Wong, Madison Sidney Virgil Quig, Issei Shinohara, Masatoshi Murayama, Simon Kwoon-Ho Chow, Bruce A Bunnell, Hang Lin and 1 more

Abstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2025. 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
–field-weighted citation impact
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.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. 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

11 authors.

Qi GaoOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: qigao7@stanford.edu.
Xiurui ZhangCenter for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. Electronic address: XIURUI@pitt.edu.
Meagan J MakarcyzkCenter for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. Electronic address: MJM392@pitt.edu.
Laurel Elizabeth WongOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: laurelwg@alumni.stanford.edu.
Madison Sidney Virgil QuigOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA; Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. Electronic address: Madisonquig@alumni.Stanford.edu.
Issei ShinoharaOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: issei27@stanford.edu.
Masatoshi MurayamaOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: muramasa@stanford.edu.
Simon Kwoon-Ho ChowOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: skhchow@stanford.edu.
Bruce A BunnellDepartment of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. Electronic address: Bruce.Bunnell@unthsc.edu.
Hang LinCenter for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. Electronic address: hal46@pitt.edu.
Stuart B GoodmanOrthopaedic Research Laboratories, Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA 94304, USA. Electronic address: goodbone@stanford.edu.

Funding

Tissue Chip Modeling of Synovial Joint Pathologies: Effects of Inflammation and Adipose-Mediated Diabetic ComplicationsUG3TR002136 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TUAN, ROCKY S · 2017 to 2018
$2.5M
Defining the unique capacity of the miniature joint model for investigating the role of adipose tissue and its impacts on osteoarthritisR01AR082386 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Bruce A. Bunnell, STUART B GOODMAN · 2024 to 2026
$1.9M
Neurophysiology of Weakness and Exercise in Rotator Cuff TendinopathyR01AR063713 · NIAMS · UNIVERSITY OF OREGON · PI KARDUNA, ANDREW ROBERT · 2014 to 2018
$1.7M
Repurposing FDA-approved drugs for the treatment of osteoarthritis using high-throughput screening in microphysiological modelsR01AR084472 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Bruce A. Bunnell, STUART B GOODMAN · 2024 to 2026
$1.6M
Customized MSCs to Enhance Healing of Bone DefectsR01AR073145 · NIAMS · STANFORD UNIVERSITY · PI GOODMAN, STUART B · 2018 to 2021
$1.4M
NCATS NIH HHS UG3 TR002136NIAMS NIH HHS R01 AR063713NIAMS NIH HHS R01 AR073145NIAMS NIH HHS R01 AR082386NIAMS NIH HHS R01 AR084472
6 · The paper itself

Abstract

objectiveTo investigate the interaction among the cells thought to be foundational to inflammation, fibrosis, and angiogenesis in the synovial membrane.

methodWe encapsulated fibroblasts, polarized macrophages, and endothelial cells in a 3D culture system. We used this model to determine the cellular transcriptional profiles, cytokine secretion, and vascular formation associated with different macrophage phenotype conditions.

resultsNeo-angiogenesis reached its maximum level at approximately day 21 in the presence of pro-inflammatory macrophages conditions, but was sustained in the presence of anti-inflammatory macrophages. RNA sequencing revealed an influence of macrophage phenotype on gene expression associated with fibrosis and angiogenesis. Furthermore, by including lipopolysaccharides-coated polyethylene particles (lcPE), an inflammatory stimulus replicating wear debris from joint replacements into our system, insights into the local reaction to byproducts of different biomaterials can be ascertained.

conclusionChronic inflammation and fibrosis of the synovial membrane are often present in osteoarthritis and post-total joint arthroplasty. Our results suggest that the progression of inflammatory synovial diseases is influenced by macrophage phenotypes.

Indexed as

FibroblastsMacrophagesNeovascularization, PathologicOrganoidsSynovial MembraneCells, CulturedEndothelial CellsFibrosisHumansPhenotype3D cultureArthroplastyImmunityParticle-induced inflammationSynovitis

Identifiers

PMID39978574
PMCPMC12182213

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.