What question did this study set out to answer?

This research aims to elucidate how acidic fibroblast growth factor (aFGF) regulates BMSCs to promote tendon-bone healing.

May 31, 2026Open Access

Multi-omics integration reveals the candidate molecular regulatory network and pathway of aFGF regulating BMSCs to promote tendon-bone healing

Key Points

This research aims to elucidate how acidic fibroblast growth factor (aFGF) regulates BMSCs to promote tendon-bone healing.
Conducted multi-omics sequencing on aFGF-treated and control BMSCs from rabbits (N=3)
Analyzed data using RNA sequencing, proteome analysis with DIA, and miRNA sequencing
Utilized GO and KEGG for analyzing differentially expressed genes and pathways
aFGF activated cell proliferation and cell cycle pathways, particularly PI3K-Akt and MAPK signaling pathways
Identified miR-29-y and NOTCH2 as key regulatory molecules involved in aFGF’s pro-healing function
Found that significant molecular changes were concentrated in synergistic regions using DIABLO analysis

Abstract

Background Acidic fibroblast growth factor (aFGF) is considered to be a key regulator for bone marrow mesenchymal stem cells (BMSCs), which are critical mediators of the tendon-bone healing process. However, how aFGF regulates BMSCs cellular behavior and promotes tendon-bone healing at multiple molecular levels has yet to be fully elucidated. Methods Based on the experimental model of aFGF-treated bone marrow mesenchymal stem cells (BMSCs) from rabbit ( Oryctolagus cuniculus ), deep multi-omics sequencing was conducted on the aFGF treatment group and the control group (n = 3), encompassing transcriptome (RNA sequencing, RNA-Seq), proteome (data-independent acquisition, DIA) and microRNA sequencing (miRNA-Seq). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the differentially expressed genes (DEGs), differentially expressed proteins (DEPs), and differentially expressed miRNA prediction genes (DEmiRPGs). Multiple omics data sets were further analyzed by Data Integration Analysis for Biomarker Discovery using Latent Components (DIABLO). The candidate regulatory axes were screened, and the enrichment analysis of related genes was assessed by GO and KEGG. Results By screening and analyzing the DEmiRPGs/DEGs/DEPs in aFGF-treated BMSCs and control BMSCs, aFGF activated several pathways, including cell proliferation, cell cycle, phosphatidylinositide 3-kinases (PI3K)-protein kinase B (Akt) signaling pathway, mitogen-activated protein kinase (MAPK) signaling pathway, and extracellular matrix (ECM)-receptor interaction. DIABLO analysis showed that most of the significantly changed molecules were located in the synergistic up/down regions. Through the screening of candidate regulatory axis, the key regulatory axis of miR-29-y/notch homolog 2 (NOTCH2) was identified in this study, which may be one of the core mechanisms of aFGF’s pro-healing function. Conclusion This study identifies the miR-29-y/NOTCH2 axis as a key regulatory hub in aFGF-treated BMSCs in vitro , potentially mediating the activation of proliferation pathways such as PI3K-Akt. These findings provide a molecular framework and generate testable hypotheses for future in vivo investigations into aFGF-mediated tendon-bone healing.

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Liu et al. (Fri,) studied this question.

synapsesocial.com/papers/6a1bcfe15783ba022b6fbc54 https://doi.org/https://doi.org/10.1016/j.lddd.2026.100417

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