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Inhibition of CRLF1 expression by miR-8485 alleviates IL-1β-induced chondrocyte inflammation, apoptosis, and extracellular matrix degradation. | LitMetric

Inhibition of CRLF1 expression by miR-8485 alleviates IL-1β-induced chondrocyte inflammation, apoptosis, and extracellular matrix degradation.

Int Immunopharmacol

Department of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China; National Clinical Research Center for Geriatric Disorders, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. Electronic address:

Published: January 2025

AI Article Synopsis

  • * Downregulation of miR-8485 leads to decreased cell activity, increased cell death, and changes in protein levels that promote inflammation and degrade cartilage.
  • * MiR-8485 suppresses inflammation by targeting CRLF1, which, when overexpressed, can counteract the anti-inflammatory effects of miR-8485, and it also inhibits critical signaling pathways (MAPK/ERK and PI3K/AKT) involved in inflammation.

Article Abstract

The aim of this study was to investigate the impact of differentially expressed miR-8485 on chondrocyte inflammation in osteoarthritis (OA) and its underlying pathological mechanisms. MiR-8485, which was downregulated in OA, was identified by microarray analysis, and was also found to be decreased in IL-1β-induced C28/I2 cells. miR-8485 down-regulation or IL-1β treated of C28/I2 cells induces a decrease in cellular activity, an increase in apoptosis, an elevation in Cleaved caspase-3, MMP13, and ADAMTS5 protein levels, a decrease in Collagen II and Aggrecan levels, and an increase in the levels of pro-inflammatory factors TNF-α and IL-6. CRLF1 was identified to be a downstream target gene of miR-8485 using bioinformatics prediction and dual luciferase reporter gene assays. CRLF1 was shown to be increased in IL-1β-treated C28/I2 cells, and CRLF1 overexpression partially abrogated the suppressive effect of upregulated miR-8485 on chondrocyte inflammation. In addition, miR-8485 was able to inhibit MAPK/ERK and PI3K/AKT signaling activation by inhibiting CRLF1. In conclusion, miR-8485 was able to inhibit CRLF1 expression and thus inhibit IL-1β-triggered inflammation in chondrocytes, potentially through the inhibition of MAPK/ERK and PI3K/AKT signaling pathways.

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Source
http://dx.doi.org/10.1016/j.intimp.2024.113643DOI Listing

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