Evidence map›Paper›PMID 37296277›Full record

ArticleScientific reports2023

Exogenously delivered iPSCs disrupt the natural repair response of endogenous MPCs after bone injury.

Leah Ferrie, Priyatha Premnath, Alexandra Olsen, Leila Larijani, Bryce A Besler, Derrick E Rancourt, Neil A Duncan, T Michael Underhill, Roman J Krawetz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. p21 Knockdown as a Therapeutic Strategy for Focal Cartilage Injury Repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
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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 3 institutions in 2 countries.

Leah FerrieMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Priyatha PremnathMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Alexandra OlsenMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Leila LarijaniMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Bryce A BeslerMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Derrick E RancourtMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
Neil A DuncanMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada.
T Michael UnderhillDepartment of Cellular and Physiological Sciences, University of British Columbia, Vancouver, BC, Canada.
Roman J KrawetzMcCaig Institute for Bone and Joint Health, University of Calgary, Calgary, AB, Canada. rkrawetz@ucalgary.ca.
Alberta Bone and Joint Health Institute · CAUniversity of Calgary · CAUniversity of British Columbia · CA

Funding

CIHR
6 · The paper itself

Abstract

Promoting bone healing including fracture non-unions are promising targets for bone tissue engineering due to the limited success of current clinical treatment methods. There has been significant research on the use of stem cells with and without biomaterial scaffolds to treat bone fractures due to their promising regenerative capabilities. However, the relative roles of exogenous vs. endogenous stem cells and their overall contribution to in vivo fracture repair is not well understood. The purpose of this study was to determine the interaction between exogenous and endogenous stem cells during bone healing. This study was conducted using a standardized burr-hole bone injury model in a mesenchymal progenitor cell (MPC) lineage-tracing mouse under normal homeostatic and osteoporotic conditions. Burr-hole injuries were treated with a collagen-I biomaterial loaded with and without labelled induced pluripotent stem cells (iPSCs). Using lineage-tracing, the roles of exogenous and endogenous stem cells during bone healing were examined. It was observed that treatment with iPSCs resulted in muted healing compared to untreated controls in intact mice post-injury. When the cell populations were examined histologically, iPSC-treated burr-hole defects presented with a dramatic reduction in endogenous MPCs and cell proliferation throughout the injury site. However, when the ovaries were removed and an osteoporotic-like phenotype induced in the mice, iPSCs treatment resulted in increased bone formation relative to untreated controls. In the absence of iPSCs, endogenous MPCs demonstrated robust proliferative and osteogenic capacity to undertake repair and this behaviour was disrupted in the presence of iPSCs which instead took on an osteoblast fate but with little proliferation. This study clearly demonstrates that exogenously delivered cell populations can impact the normal function of endogenous stem/progenitor populations during the normal healing cascade. These interactions need to be better understood to inform cell and biomaterial therapies to treat fractures.

Indexed as

Induced Pluripotent Stem CellsMesenchymal Stem CellsAnimalsBiocompatible MaterialsCell DifferentiationMiceOsteogenesisTissue EngineeringBiocompatible Materials

Identifiers

PMID37296277
PMCPMC10256810
OpenAlexW4380084604

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.