Evidence map›Paper›PMID 40264197›Full record

ArticleStem cell research & therapy2025

LncRNA MRF targeting FSHR inhibits the osteogenic differentiation of BMSCs and bone defect repair through the regulation of the cAMP-PKA-CREB signaling pathway.

Qing Ning, Ming Li, Zhuangyao Liao, Enming Chen, Huatao Liu, Yuwei Liang, Yuanquan Chen, Yuxi Li, Lin Huang

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. The long non-coding RNAFrontiers in nutrition · 2026
    Article
  4. 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

9 authors.

Qing NingDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Ming LiDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Zhuangyao LiaoDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Enming ChenDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Huatao LiuDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Yuwei LiangDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Yuanquan ChenDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China.
Yuxi LiDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China. liyx73@mail.sysu.edu.cn.
Lin HuangDepartment of Orthopedics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, People's Republic of China. huangl5@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-8285-2658

Funding

Guangzhou Science and technology planning project 202201010881Natural Science Foundation of Guangdong Province 2021A1515111013Natural Science Foundation of Guangdong Province 2022A1515012305
6 · The paper itself

Abstract

backgroundMesenchymal stem cells (MSCs), known for their ability to differentiate into osteoblasts, play a pivotal role in bone metabolism. In our previous investigations, we identified a novel long non-coding RNA (lncRNA) named MCP1 Regulatory Factor (MRF), which exhibits significant involvement in immune regulation of BMSCs. Moreover, we observed noticeable expression changes of MRF during the osteogenic differentiation of BMSCs. However, the exact role and underlying mechanism of MRF in the osteogenic differentiation of BMSCs remain elusive.

methodsQRT-PCR analysis was employed to assess the expression levels of MRF. RNA interference and overexpression plasmids were utilized to modulate MRF expression, allowing for the observation of changes in the osteogenic differentiation capacity of BMSCs. Downstream pathways involved in the MRF-mediated regulation of BMSCs' osteogenic differentiation were predicted using transcriptome sequencing. The functionality of MRF in vivo was validated through a mouse tibial drilling defect model.

resultsIn patients with osteoporosis, there is a notable increase in the expression of MRF within BMSCs. During the osteogenic differentiation of BMSCs, the MRF expression progressively decreases. The knockdown of MRF significantly enhances the osteogenic differentiation of BMSCs, promoting an increased expression of bone-related proteins such as RUNX2, ALP, and COL1A1. Transcriptome sequencing and western blot indicated that cAMP/PKA/CREB signaling pathway was significantly activated after lncRNA-MRF knockdown. Moreover, in the mouse tibial drilling defect model, MRF knockdown significantly promotes ossification in vivo.

conclusionsMRF modulates the cAMP/PKA/CREB signaling pathway via the follicle stimulating hormone receptor (FSHR), thereby influencing the ossification differentiation of BMSCs. Our research suggests that MRF may serve as a potential target for bone-related disorders.

Indexed as

Mesenchymal Stem CellsOsteogenesisReceptors, FSHRNA, Long NoncodingAnimalsCell DifferentiationCells, CulturedCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinFemaleHumansMaleMiceOsteoporosisSignal TransductionCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinReceptors, FSHRNA, Long NoncodingBMSCsFSHRLncRNAMRFOsteogenesis

Identifiers

PMID40264197
PMCPMC12016372

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Registered trials

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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.