These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: MiR-379-5p Promotes Chondrocyte Proliferation via Inhibition of PI3K/Akt Pathway by Targeting YBX1 in Osteoarthritis.
    Author: Zhang H, Zheng W, Li D, Zheng J.
    Journal: Cartilage; 2022; 13(1):19476035221074024. PubMed ID: 35255737.
    Abstract:
    OBJECTIVE: We evaluated the ability of miR-379-5p to influence the proliferation of osteoarthritis chondrocytes and elucidated the regulatory mechanism of miR-379-5p in osteoarthritis. METHODS: Real time polymerase chain reaction (RT- PCR) was used to detect the expression of miR-379-5p and YBX1 in knee articular cartilages of human. Cell proliferation, inflammatory factors, extracellular matrix (ECM) degradation-associated proteins and proteins in PI3K/Akt pathway were assessed in rat primary chondrocytes treated with interleukin (IL)-1β or/and miR-379-5p mimics or miR-379-5p inhibitor via cell counting assay kit-8 (CCK-8), enzyme-linked immunosorbent assay (ELISA), immunofluorescence and Western blotting (WB). The target of miR-379-5p predicted by TargetScan and miRwalk software was verified by luciferase reporter assay. Safranin O-fast green staining, immunohistochemistry, and WB were performed to observe the effect of miR-379-5p agomir on development of osteoarthritis in rats. RESULTS: MiR-379-5p was down-regulated in human osteoarthritic tissues and negatively correlated with YBX1 expression. High level of miR-379-5p in chondrocytes with IL-1β stimulated increased cell viability, the expression of proliferation-related protein and extracellular matrix (ECM)-related proteins collagen II and aggrecan. However, the expression of inflammatory factors and ECM-related proteins matrix metalloproteinases (MMP-1) and MMP-13 was decreased. Luciferase reporting assay verified the targeting relationship between miR-379-5p and YBX1. This function of miR-379-5p was exerted through PI3K/Akt pathway and could be blocked by the PI3K/Akt pathway inhibitor LY294002. MiR-379-5p agomir promoted the articular chondrocytes proliferation and alleviated cartilage degradation in vivo. CONCLUSION: Our findings reveal that miR-379-5p can promote the articular chondrocytes proliferation in osteoarthritis (OA) by interacting with YBX1 and regulating PI3K/Akt pathway. Restoring miR-379-5p might be a future therapeutic strategy for OA.
    [Abstract] [Full Text] [Related] [New Search]