Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management.

Yang Wang, Dong Wei, Zhineng Chen, Liang Zhong

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Article in Journal of musculoskeletal & neuronal interactions, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed

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1 citing paper in PubMed.

Multi-Breed Genome-Wide Association Analysis Reveals Candidate Genes for Growth and Body Conformation Traits in Four Populations of Native and Crossbred Chinese Sheep.Animals : an open access journal from MDPI · 2026
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4 authors.

Yang WangDepartment of Traditional Chinese Orthopedics, Hangzhou Xiaoshan District Traditional Chinese Medicine Hospital, Zhejiang, China.

Dong WeiDepartment of Traditional Chinese Orthopedics, Hangzhou Xiaoshan District Traditional Chinese Medicine Hospital, Zhejiang, China.

Zhineng ChenDepartment of Traditional Chinese Orthopedics, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang, China.

Liang ZhongDepartment of Traditional Chinese Orthopedics, Hangzhou Xiaoshan District Traditional Chinese Medicine Hospital, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesOsteoporosis (OP) is a prevalent bone disease characterized by reduced bone mass and increased fracture risk, in part due to impaired osteogenic differentiation of bone marrow-derived mesenchymal stromal cells (BMSCs). Loss of AT-rich interactive domain-containing protein 2 (ARID2) attenuates BMSC osteogenesis, but the underlying mechanism remains to be elucidated.

methodsHuman BMSCs were induced to undergo osteogenic or adipogenic differentiation. Lentiviral transduction was used to silence ARID2 and/or overexpress serine/threonine kinase 39 (STK39). Effects on BMSC fate were assessed by quantitative reverse-transcription PCR (qRT-PCR), MTT assay, alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, Oil Red O staining, and western blotting.

resultsARID2 expression increased over time during osteogenic induction. ARID2 silencing reduced BMSC proliferation and osteogenic differentiation while favoring adipogenesis. Conversely, STK39 overexpression enhanced proliferation and osteogenic differentiation and attenuated nuclear factor κB (NF-κB) signaling during osteogenic induction; these effects were reversed by ARID2 silencing.

conclusionThe STK39-ARID2 axis promotes osteogenic differentiation and suppresses adipogenic differentiation of BMSCs, at least in part via inhibition of NF-κB signaling. These findings highlight a potential molecular target for therapeutic strategies in OP.

Indexed as

Cell DifferentiationMesenchymal Stem CellsNF-kappa BOsteogenesisOsteoporosisProtein Serine-Threonine KinasesTranscription FactorsCells, CulturedHumansSignal TransductionNF-kappa BProtein Serine-Threonine KinasesTranscription FactorsAT-rich interactive domain-containing protein 2Bone marrow mesenchymal stem cellsOsteogenic differentiationOsteoporosisSerine/threonine kinase 39

Identifiers

PMID41764760

PMCPMC12952502

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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.