LncRNA MEG3-TRPV1 signaling regulates chronic inflammatory pain in rats

Osteoarthritis (OA) is a common osteoarthropathy with chronic inflammatory pain as the core symptom in middle-aged and elderly people. LncRNA MEG3 (Maternally expressed gene 3) is involved in the development of OA via regulation of angiogenesis, which causes the activation and overexpression of tran...

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Published in:Molecular pain 2022-04, Vol.18, p.17448069221144246-17448069221144246
Main Authors: Peng, Jing-Wei, Gu, Yin-Yin, Wei, Jia, Sun, Ye, Zhu, Chun-Long, Zhang, Ling, Song, Yu, Chen, Long, Chen, Xia, Wang, Qian, Zhang, Hai-Long
Format: Article
Language:English
Subjects:
Angiogenesis
Animals
Capsaicin receptors
Chronic pain
Chronic Pain - complications
Chronic Pain - genetics
Freund's Adjuvant - toxicity
Hyperalgesia - drug therapy
Inflammation
Inflammation - chemically induced
Inflammation - complications
Joint diseases
Microinjection
mRNA
Non-coding RNA
Osteoarthritis
Pain
Rats
RNA, Long Noncoding - genetics
RNA, Messenger - genetics
Therapeutic targets
Transient receptor potential proteins
TRPV Cation Channels - genetics
TRPV Cation Channels - metabolism
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Summary:Osteoarthritis (OA) is a common osteoarthropathy with chronic inflammatory pain as the core symptom in middle-aged and elderly people. LncRNA MEG3 (Maternally expressed gene 3) is involved in the development of OA via regulation of angiogenesis, which causes the activation and overexpression of transient receptor potential vanilloid type-1 (TRPV1). In this study, we investigated the mechanism of MEG3-TRPV1 signaling in chronic inflammatory pain (CIP) of rat model. Chronic inflammatory pain was modeled using subcutaneous microinjection of complete Freund’s adjuvant (CFA) into the left hind paw of rats. We showed that TRPV1 mRNA and protein were significantly increased, while MEG3 mRNA was significantly decreased, in the DRG and SDH of CFA-induced rats. In addition, intrathecal injection of MEG3-overexpressing lentivirus significantly downregulated TRPV1 expression and alleviated chronic inflammatory pain in CFA-induced rats. Treatment with a TRPV1 antagonist also significantly relieved chronic inflammatory pain in CFA-induced rats. In general, our results reveal that MEG3 alleviates chronic inflammatory pain by downregulating TRPV1 expression. These findings may provide new therapeutic targets in the treatment of patients with OA.
ISSN:1744-8069
1744-8069
DOI:10.1177/17448069221144246