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Updated: Jun 26, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Knocking-down long non-coding RNA LINC01094 prohibits chondrocyte apoptosis via regulating
Feiri Huang1,2, Zhongliang Su2, Jie Yang2
1Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou, China.
Purpose:
The abnormal function and survival of chondrocytes result in articular cartilage failure, which may accelerate the onset and development of osteoarthritis (OA). This study is aimed to investigate the role of LINC01094 in chondrocyte apoptosis.
Methods:
The viability and apoptosis of lipopolysaccharide (LPS)-induced chondrocytes were evaluated through CCK-8 assay and flow cytometry analysis, respectively. The expression levels of LINC01094, miR-577 and MTF1 were detected by qRT-PCR. Dual luciferase reporter tests were implemented for the verification of targeted relationships among them. Western blotting was employed to measure the levels of pro-apoptotic proteins (Caspase3 and Caspase9).
Results:
The viability of LPS-induced chondrocytes was overtly promoted by loss of LINC01094 or miR-577 upregulation, but could be repressed via MTF1 overexpression. The opposite results were observed in apoptosis rate and the levels of Caspase3 and Caspase9. LINC01094 directly bound to miR-577, while MTF1 was verified to be modulated by miR-577. Both LINC01094 and MTF1 were at high levels, whereas miR-577 was at low level in OA synovial fluid and LPS-induced chondrocytes. Furthermore, the highly expressed miR-577 abolished the influences of MTF1 overexpression on LPS-induced chondrocytes.
Conclusions:
Silencing of LINC01094 represses the apoptosis of chondrocytes through upregulating miR-577 expression and downregulating MTF1 levels, providing a preliminary insight for the treatment of OA in the future.
Insights
Silencing LINC01094 reduces chondrocyte apoptosis by increasing miR-577 and decreasing MTF1. This finding offers potential therapeutic strategies for osteoarthritis (OA) by targeting chondrocyte dysfunction.
Area of Science:
- Biomedical Science
- Molecular Biology
- Cell Biology
Background:
- Abnormal chondrocyte function and survival contribute to articular cartilage failure and osteoarthritis (OA) development.
- Understanding the molecular mechanisms regulating chondrocyte apoptosis is crucial for OA pathogenesis research.
Purpose of the Study:
- To investigate the role of long non-coding RNA LINC01094 in regulating chondrocyte apoptosis.
- To elucidate the molecular interactions between LINC01094, miR-577, and MTF1 in the context of OA.
Main Methods:
- Assessing chondrocyte viability and apoptosis using CCK-8 assay and flow cytometry.
- Quantifying gene expression levels of LINC01094, miR-577, and MTF1 via qRT-PCR.
- Verifying molecular interactions using dual luciferase reporter assays and Western blotting for apoptosis-related proteins.
Main Results:
- LINC01094 and MTF1 were upregulated, while miR-577 was downregulated in OA synovial fluid and LPS-induced chondrocytes.
- LINC01094 directly targets miR-577, and miR-577 modulates MTF1 expression.
- Silencing LINC01094 promoted chondrocyte viability and reduced apoptosis by upregulating miR-577 and downregulating MTF1.
Conclusions:
- LINC01094 silencing inhibits chondrocyte apoptosis via the miR-577/MTF1 axis.
- This study provides a potential molecular target for future osteoarthritis therapeutic interventions.
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