Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis
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1The Joint Surgical Center, Chenzhou No. 1 People's Hospital, Chenzhou, Hunan 423000, China. hexiao8211@163.com.
Introduction:
Osteoarthritis (OA) is the most prevailing musculoskeletal dysfunction triggered by lesions in synovial membranes and articular cartilage. MicroRNAs (miRNAs) have emerged as crucial regulators participated in many biological processes, such as osteoarthritis. This study was undertaken to address the role of miR-25-3p in the apoptosis of rat chondrocytes under an OA-like condition and its underlying mechanism.
Material And Methods:
OA cellular model was established in rat chondrocytes by TNF-a induction. Then, qRTPCR and Western blotting were utilized for evaluation of the expressions of miR-25-3p and insulin-like growth factor-binding protein 7 (IGFBP7), CCK-8 assay for inspection of chondrocyte viability, flow cytometry for assessment of cell apoptosis rate, Western blotting for the detection of cleaved caspase-3 level and dual-luciferase reporter gene assay for verification of the targeting relationship between miR-25-3p and IGFBP7.
Results:
The miR-25-3p expression was decreased and IGFBP7 was elevated in TNF-a-induced rat chondrocytes. The miR-25-3p inhibited chondrocyte apoptosis and IGFBP7 promoted apoptosis as evidenced by enhanced cell viability and suppressed cell apoptosis in OA chondrocytes after miR-25-3p overexpression or IGFBP7 knockdown. The miR-25-3p facilitated chondrocyte viability and repressed cell apoptosis in OA by negatively regulating IGFBP7.
Conclusions:
MiR-25-3p negatively regulates IGFBP7 to promote chondrocyte proliferation and restrain chondrocyte apoptosis. Our findings suggest that the regulation of IGFBP7 by miR-25-3p may emerge as a novel therapeutic regimen for OA.
Insights
MicroRNA-25-3p inhibits osteoarthritis progression by reducing chondrocyte apoptosis and lowering IGFBP7 levels. This suggests miR-25-3p as a potential therapeutic target for osteoarthritis treatment.
Area of Science:
- Molecular Biology
- Biochemistry
- Genetics
Background:
- Osteoarthritis (OA) is a prevalent musculoskeletal disorder affecting synovial membranes and articular cartilage.
- MicroRNAs (miRNAs) play a critical role in regulating biological processes, including those involved in osteoarthritis pathogenesis.
Purpose of the Study:
- To investigate the role of miR-25-3p in rat chondrocyte apoptosis under osteoarthritis-like conditions.
- To elucidate the underlying molecular mechanism involving insulin-like growth factor-binding protein 7 (IGFBP7).
Main Methods:
- Established an OA cellular model using TNF-α induction in rat chondrocytes.
- Quantified miR-25-3p and IGFBP7 expression using qRT-PCR and Western blotting.
- Assessed chondrocyte viability, apoptosis rates, and caspase-3 levels, and verified the miR-25-3p/IGFBP7 interaction via dual-luciferase reporter assay.
Main Results:
- miR-25-3p expression was decreased, while IGFBP7 expression was elevated in TNF-α-induced chondrocytes.
- Overexpression of miR-25-3p inhibited chondrocyte apoptosis and enhanced viability.
- IGFBP7 promoted apoptosis, and its knockdown suppressed apoptosis in OA chondrocytes.
Conclusions:
- miR-25-3p negatively regulates IGFBP7, thereby promoting chondrocyte proliferation and inhibiting apoptosis.
- Targeting the miR-25-3p/IGFBP7 axis presents a potential novel therapeutic strategy for osteoarthritis.
