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Updated: Nov 4, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Hsa_circ_0032131 knockdown inhibits osteoarthritis progression via the miR-502-5p/PRDX3 axis
Jin Xu1, Xinlong Ma1
1Department of Pain Treatment, Tianjin Hospital, Tianjin 300211, China.
Abstract:
Osteoarthritis (OA) is a chronic disease characterized by progressive loss of cartilage and failure of the diarthrodial joint. Circular RNAs (circRNAs) are known to participate in the pathogenesis of multiple diseases, including OA. We investigated the functions of hsa_circ_0032131, a circRNA upregulated in OA, using CHON-001 cells and an in vivo OA rat model. CHON-001 cells were treated with interleukin (IL)-1β to mimic OA in vitro. IL-1β-induced inhibition of CHON-001 growth was reversed by silencing hsa_circ_0032131. In addition, hsa_circ_0032131 knockdown reversed IL-1β-induced activation of Trx1, Cyclin D and PRDX3, whereas overexpression of PRDX3, a direct target of miR-502-5p, reversed this effect. Hsa_circ_0032131 served as a competing endogenous RNA for miR-502-5p. Moreover, knockdown of hsa_circ_0032131 attenuated OA symptoms in vivo by inactivating the STAT3 signaling pathway. Thus, silencing of hsa_circ_0032131 inhibited the progression of OA by inactivating the miR-502-5p/PRDX3/Trx1/STAT3 axis, which highlights its potential as a therapeutic target for OA.
Insights
Silencing hsa_circ_0032131, a circular RNA, inhibits osteoarthritis progression. This occurs by targeting the miR-502-5p/PRDX3/Trx1/STAT3 pathway, suggesting hsa_circ_0032131 as a potential therapeutic target for osteoarthritis.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Osteoarthritis (OA) is a degenerative joint disease involving cartilage loss.
- Circular RNAs (circRNAs) are implicated in various disease pathologies, including OA.
- Hsa_circ_0032131 is a circRNA found to be upregulated in osteoarthritis.
Purpose of the Study:
- To investigate the functional role of hsa_circ_0032131 in osteoarthritis.
- To elucidate the molecular mechanisms underlying hsa_circ_0032131's involvement in OA pathogenesis.
- To evaluate hsa_circ_0032131 as a potential therapeutic target for OA.
Main Methods:
- Utilized CHON-001 cells treated with interleukin-1 beta (IL-1β) to model OA in vitro.
- Performed gene silencing and overexpression experiments for hsa_circ_0032131 and PRDX3.
- Employed an in vivo osteoarthritis rat model to assess therapeutic effects.
Main Results:
- Silencing hsa_circ_0032131 reversed IL-1β-induced inhibition of CHON-001 cell growth.
- Hsa_circ_0032131 acts as a competing endogenous RNA for miR-502-5p.
- Knockdown of hsa_circ_0032131 attenuated OA symptoms in vivo by inactivating the STAT3 signaling pathway.
Conclusions:
- Hsa_circ_0032131 promotes osteoarthritis progression through the miR-502-5p/PRDX3/Trx1/STAT3 axis.
- Silencing hsa_circ_0032131 demonstrates therapeutic potential for osteoarthritis.
- Targeting hsa_circ_0032131 offers a novel strategy for OA treatment.
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