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Published on: February 6, 2017
MicroRNA‑143‑3p contributes to the regulation of pain responses in collagen‑induced arthritis
Ling-Ling Zhou1, Ya-Mei Zhu1, Fei-Ya Qian1
1School of Pharmacy, The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P.R. China.
Abstract:
Patients with rheumatoid arthritis (RA) suffer from pain, which is associated with inflammation, peripheral and central pain processing, and joint structure damage. The aim of the present study was to investigate a key microRNA (miR) and its target genes that are involved in the pain responses of RA, and to clarify the mechanism of pain regulation. Collagen‑induced arthritis (CIA) was induced in DBA/1 and C57BL/6 mice. The paw swelling, mechanical withdrawal threshold (MWT), thermal withdrawal latency (TWL), and expression levels of tumor necrosis factor (TNF)‑α and prostaglandin (PG)E2 in the sera were investigated. Decreased MWT and TWL, and increased TNF‑α and PGE2, in the CIA model group were observed in DBA/1 and C57BL/6 mice. DBA/1 mice exhibited greater hyperalgesia and higher levels of inflammatory mediators. miR‑143‑3p expression in the blood and the dorsal root ganglion (DRG) were detected, and low miR‑143‑3p expression was demonstrated in the blood and DRG tissue of CIA mice. The target genes of miR‑143 were predicted and analyzed. A total of 1,305 genes were predicted and 55 pain‑associated genes were obtained. Prostaglandin‑endoperoxide synthase 2 (Ptgs2), MAS related GPR family member E (Mrgpre), prostaglandin D2 receptor and Tnf were selected as target genes of miR‑143. DRG cells were cultured and transfected with miR‑143‑3p inhibitor or mimic. The expression of Mrgpre, Ptgs2 and Tnf was significantly inhibited following miR‑143‑3p mimic transfection, while the expression of Mrgpre, Ptgs2 and Tnf was increased following inhibitor transfection. Additionally, the expression of pain‑associated genes in the DRG of mice was investigated and the expression of Ptgs2, Mrgpre and Tnf in the DRG of CIA mice was also significantly upregulated. These results revealed that CIA mice exhibited marked hyperalgesia and high levels of inflammatory pain mediators. Low expression of miR‑143‑3p negatively regulated the pain‑associated target genes, including Mrgpre, Ptgs2 and Tnf, thereby affecting chronic inflammatory pain and neuropathic pain in RA.
Insights
Low expression of microRNA-143-3p (miR-143-3p) is linked to increased pain in rheumatoid arthritis (RA). This study identifies miR-143-3p as a regulator of pain-associated genes, offering potential therapeutic targets for RA pain.
Area of Science:
- Biomedical Science
- Molecular Biology
- Pain Research
Background:
- Rheumatoid arthritis (RA) patients experience significant pain due to inflammation and altered pain processing.
- Understanding the molecular mechanisms underlying RA pain is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of a specific microRNA (miR-143-3p) in the pain responses associated with rheumatoid arthritis.
- To identify and analyze the target genes regulated by miR-143-3p involved in RA pain mechanisms.
Main Methods:
- Collagen-induced arthritis (CIA) mouse model was used to study pain behaviors and inflammatory markers.
- Expression levels of miR-143-3p and its target genes (e.g., Ptgs2, Mrgpre, Tnf) were analyzed in blood and dorsal root ganglion (DRG) tissues.
- In vitro transfection of DRG cells with miR-143-3p mimics or inhibitors was performed.
Main Results:
- CIA mice showed increased hyperalgesia, paw swelling, and elevated levels of inflammatory mediators (TNF-α, PGE2).
- A significant downregulation of miR-143-3p was observed in the blood and DRG of CIA mice.
- miR-143-3p mimic transfection inhibited target gene expression, while inhibitor transfection increased it, confirming its regulatory role.
Conclusions:
- Low miR-143-3p expression contributes to RA-associated pain by upregulating target genes like Mrgpre, Ptgs2, and Tnf.
- miR-143-3p represents a potential therapeutic target for managing chronic inflammatory and neuropathic pain in rheumatoid arthritis.
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