eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
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abstract:
Original paper

LncRNA RMRP promotes chondrocyte injury by regulating the FOXC1/RBP4 axis

Jingyi Li
1
,
Gang Zhou
1
,
Te Chen
1
,
Qiao Lin
1
,
Qiupeng Yang
1

  1. Joint Surgical Department, Hainan General Hospital, Haikou 570100, Hainan Province, P.R. China
Cent Eur J Immunol 2024; 49 (4)
DOI: https://doi.org/10.5114/ceji.2024.145312
Online publish date: 2024/12/06
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Introduction:
The main pathological feature of osteoarthritis (OA) is chondrocyte injury. LncRNA mitochondrial RNA processing endoribonuclease (RMRP) has been shown to be a chondrogenic differentiation factor. This study aimed to explore the role of RMRP in chondrocyte injury.

Material and methods:
Cell counting kit-8 (CCK-8) and TUNEL assays were used to determine lipopolysaccharide (LPS)-induced chondrocyte viability and apoptosis, respectively. The interaction between RMRP and FOXC1 was analyzed by RIP and RNA pull-down. Dual luciferase reporter and ChIP were employed to analyze the interaction between FOXC1 and RBP4. The levels of RMRP, FOXC1, RBP4, apoptosis-related and extracellular matrix (ECM)-related genes were detected by RT-qPCR and western blot. ELISA assay was used for detection of inflammatory cytokines in LPS-induced chondrocytes.

Results:
The levels of RMRP, FOXC1 and RBP4 were significantly upregulated in OA cartilage tissues and LPS-induced chondrocytes. Knockdown of RMRP inhibited chondrocyte apoptosis and inflammation under LPS. RMRP interacted with FOXC1 and promoted RBP4 expression. FOXC1 could upregulate RBP4 and promote LPS-induced chondrocyte apoptosis and inflammation. Similarly, RMRP combined with FOXC1 and aggravated apoptosis and inflammation in LPS-treated chondrocytes.

Conclusions:
RMRP promoted upregulation of RBP4 and activation of the JNK signaling pathway by binding to FOXC1, thereby accelerating LPS-induced apoptosis and inflammation in chondrocytes.

keywords:

osteoarthritis, chondrocyte injury, lncRNA RMRP, FOXC1, RBP4
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