Evidence map›Paper›PMID 38951811›Full record

ArticleJournal of orthopaedic surgery and research2024

T. gondii excretory proteins promote the osteogenic differentiation of human bone mesenchymal stem cells via the BMP/Smad signaling pathway.

Mingzhu Deng, Feifei Gao, Tianfeng Liu, Weiqiang Zhan, Juanhua Quan, Ziquan Zhao, Xuyang Wu, Zhuolan Zhong, Hong Zheng, Jiaqi Chu

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In one paragraph

Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
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

10 authors.

Mingzhu Deng *Orthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Feifei Gao *Stem Cell Research and Cellular Therapy Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Tianfeng LiuStem Cell Research and Cellular Therapy Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Weiqiang ZhanOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Juanhua QuanLaboratory of Gastroenterology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Ziquan ZhaoOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Xuyang WuOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Zhuolan ZhongOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Hong ZhengOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China. zhenghong@gdmu.edu.cn.
Jiaqi ChuOrthopaedic Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China. chujiaqi@gdmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBone defects, resulting from substantial bone loss that exceeds the natural self-healing capacity, pose significant challenges to current therapeutic approaches due to various limitations. In the quest for alternative therapeutic strategies, bone tissue engineering has emerged as a promising avenue. Notably, excretory proteins from Toxoplasma gondii (TgEP), recognized for their immunogenicity and broad spectrum of biological activities secreted or excreted during the parasite's lifecycle, have been identified as potential facilitators of osteogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs). Building on our previous findings that TgEP can enhance osteogenic differentiation, this study investigated the molecular mechanisms underlying this effect and assessed its therapeutic potential in vivo.

methodsWe determined the optimum concentration of TgEP through cell cytotoxicity and cell proliferation assays. Subsequently, hBMSCs were treated with the appropriate concentration of TgEP. We assessed osteogenic protein markers, including alkaline phosphatase (ALP), Runx2, and Osx, as well as components of the BMP/Smad signaling pathway using quantitative real-time PCR (qRT-PCR), siRNA interference of hBMSCs, Western blot analysis, and other methods. Furthermore, we created a bone defect model in Sprague-Dawley (SD) male rats and filled the defect areas with the GelMa hydrogel, with or without TgEP. Microcomputed tomography (micro-CT) was employed to analyze the bone parameters of defect sites. H&E, Masson and immunohistochemical staining were used to assess the repair conditions of the defect area.

resultsOur results indicate that TgEP promotes the expression of key osteogenic markers, including ALP, Runx2, and Osx, as well as the activation of Smad1, BMP2, and phosphorylated Smad1/5-crucial elements of the BMP/Smad signaling pathway. Furthermore, in vivo experiments using a bone defect model in rats demonstrated that TgEP markedly promoted bone defect repair.

conclusionOur results provide compelling evidence that TgEP facilitates hBMSC osteogenic differentiation through the BMP/Smad signaling pathway, highlighting its potential as a therapeutic approach for bone tissue engineering for bone defect healing.

Indexed as

Cell DifferentiationMesenchymal Stem CellsOsteogenesisRats, Sprague-DawleySignal TransductionToxoplasmaAnimalsBone Morphogenetic ProteinsCells, CulturedHumansMaleProtozoan ProteinsRatsSmad ProteinsBone Morphogenetic ProteinsProtozoan ProteinsSmad ProteinsBMP/Smad signaling pathwayBone defectBone marrow mesenchymal stem cellsExcretory proteinsOsteogenic differentiationToxoplasma gondii

Identifiers

PMID38951811
PMCPMC11218376

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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.