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Updated: Jun 21, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Silencing of CircTRIM25/miR-138-5p/CREB1 axis promotes chondrogenesis in osteoarthritis
Chunlei He1, Zhaogan Zeng2, Yadong Yang1
1Department of Orthopedics, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Background:
Dysregulated circular RNAs (circRNAs) are involved in osteoarthritis (OA) progression.
Objective:
We aimed to explore the effect of hsa_circ_0044719 (circTRIM25) on the ferroptosis of chondrocytes.
Methods:
Chondrocytes were treated with interleukin (IL)-1β to generate cell model. Cellular behaviours were measured using cell counting kit-8, enzyme-linked immunosorbent assay, relevant kits, propidium iodide staining, and immunofluorescence assay. Quantitative real-time polymerase chain reaction was performed to examine the expression of circTRIM25, miR-138-5p, and cAMP responsive element binding protein 1 (CREB1), and their interactions were assessed using luciferase reporter analysis and RNA pull-down assay.
Results:
CircTRIM25 was upregulated in OA tissues and IL-1β-stimulated chondrocytes. Knockdown of circTRIM25 facilitated the viability and suppressed ferroptosis and inflammation of IL-1β-induced cells. CircTRIM25 served as a sponge of miR-138-5p, which directly targets CREB1. Downregulation of miR-138-5p abrogated the effect induced by knockdown of circTRIM25. Furthermore, enforced CREB1 reversed the miR-138-5p induced effect. Moreover, knockdown of circTRIM25 attenuated cartilage injury in vivo.
Conclusion:
Silencing of circTRIM25 inhibited ferroptosis of chondrocytes via the miR-138-5p/CREB axis and thus attenuated OA progression.
Insights
Silencing circular RNA TRIM25 (circTRIM25) inhibits chondrocyte ferroptosis and inflammation, thereby slowing osteoarthritis progression. This occurs through the miR-138-5p/CREB pathway, offering a potential therapeutic target for OA.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Dysregulated circular RNAs (circRNAs) are implicated in osteoarthritis (OA) pathogenesis.
- Investigating specific circRNAs like hsa_circ_0044719 (circTRIM25) is crucial for understanding OA progression.
Purpose of the Study:
- To elucidate the role of circTRIM25 in chondrocyte ferroptosis.
- To explore the underlying molecular mechanisms involving miR-138-5p and CREB1.
Main Methods:
- Chondrocytes were stimulated with IL-1β to model OA.
- Quantitative real-time PCR, luciferase reporter assays, and RNA pull-down assays were used to analyze gene expression and interactions.
- Cellular viability, ferroptosis, and inflammation markers were assessed using various assays.
Main Results:
- CircTRIM25 expression was elevated in OA tissues and IL-1β-treated chondrocytes.
- Knockdown of circTRIM25 reduced chondrocyte ferroptosis and inflammation, and attenuated cartilage damage in vivo.
- CircTRIM25 acts as a sponge for miR-138-5p, which targets CREB1, revealing a regulatory axis.
Conclusions:
- Silencing circTRIM25 ameliorates OA by inhibiting chondrocyte ferroptosis via the circTRIM25/miR-138-5p/CREB1 pathway.
- CircTRIM25 represents a potential therapeutic target for osteoarthritis treatment.
