Evidence map›Paper›PMID 41689041›Full record

ArticleJournal of orthopaedic surgery and research2026

LINC00312 affects the progression of osteoarthritis by targeting miR-331-3p/DUSP5 axis.

Dengke Zhao, Yiming Zhao, Yuxiang He, Cheng Wang

Abstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Dengke ZhaoDepartment of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China.
Yiming ZhaoDepartment of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China.
Yuxiang HeDepartment of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China.
Cheng WangDepartment of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China. wangchengqilu@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs a chronic degenerative disease, osteoarthritis (OA) manifests through articular cartilage breakdown and ongoing inflammatory processes in joints. Recently, long non-coding RNAs (lncRNAs) have been participated in pathological process of OA through epigenetic regulation and molecular signaling axis.

aimThis study aimed to verify whether LINC00312 regulates DUSP5 expression by adsorbing miR-331-3p as a competitive endogenous RNA (ceRNA) in OA, thereby exerting a cartilage-protective effect.

methodsExpressions of LINC00312, miR-331-3p, and dual-specific protein phosphatase 5 (DUSP5) in patient tissues and chondrocytes were detected by reverse transcription-quantitative PCR (RT-qPCR). An in vitro OA model was constructed by stimulating chondrocytes with IL-1β. Cell viability and apoptosis were assessed via cell counting kit-8 (CCK-8) assays and flow cytometry. The levels of chondrogenic-related genes and proinflammatory factors were detected by RT-qPCR and enzyme-linked immunosorbent assay (ELISA). Interaction of miR-331-3p with LINC00312 and DUSP5 was detected via dual luciferase assays and RIP assays. Correlation between LINC00312, miR-331-3p, and DUSP5 in patients with OA was analyzed using Pearson correlation analysis.

resultsIn OA patients' cartilage tissue and IL-1β-induced OA models, LINC00312 and DUSP5 expression decreased while miR-331- 3p expression increased. Overexpression of LINC00312 ameliorated cell injury induced by IL-1β stimulation, enhanced cell viability, and reduced apoptosis, MMP13, ADAMTS5, IL-6, and IL-8 levels. miR-331-3p negatively correlated with LINC00312, and upregulation of miR-331-3p reversed the protective effect of LINC00312. Additionally, DUSP5 was a direct target of miR-331-3p, and LINC00312 and miR-331-3p jointly regulated DUSP5 expression.

conclusionsLINC00312 alleviates IL-1β-induced chondrocyte inflammation and apoptosis by acting as a ceRNA to regulate the miR-331-3p/DUSP5 axis. This suggests that LINC00312 may serve as a novel therapeutic target for OA.

Indexed as

Dual-Specificity PhosphatasesMicroRNAsOsteoarthritisRNA, Long NoncodingApoptosisCells, CulturedChondrocytesDisease ProgressionGene Expression RegulationHumansInterleukin-1betaMaleDual-Specificity PhosphatasesDUSP5 protein, humanInterleukin-1betaMicroRNAsRNA, Long NoncodingChondrocytesDUSP5LINC00312miR-331-3pOsteoarthritis

Identifiers

PMID41689041
PMCPMC13005469

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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.