Abstract |
Spinal cord injury (SCI) is a neurological disease having devastating effect and results in the development of systemic inflammation. However, the molecular mechanisms of SCI remain not entirely elucidated. This study was directed toward exploring the circ Hecw1 involved in the mechanism of lipopolysaccharide (LPS)-triggered inflammation damage in neuronal cells. The in vitro model of SCI based on PC12 cells were established with lipopolysaccharide. The cell proliferation was determined by the use of cell counting kit-8 (CCK8). The expressions of circHecw1, miR-3551-3p, and inflammatory factors were measured by quantitative real-time PCR and ELISA assay. Flow cytometry was used to assess apoptosis. Western blot analysis was performed for the purpose of determining LRRTM1 and NF-kB signaling. The expression of circ Hecw1, TNF-α, IL-6, and IL-1β in LPS-triggered PC12 cells and the expression of miR-3551-3p and IL-10 were significantly decreased. Knockdown of circHecw1 promoted proliferation and inhibited apoptosis and reduction in the inflammatory cytokine expression. Our study revealed that circHecw1 regulates SCI neuronal cell inflammation imbalance by regulating the miR-3551-3p/LRRTM1 signaling.
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Authors | Dexiang Ban, Zhenyang Xiang, Peng Yu, Yang Liu |
Journal | Applied biochemistry and biotechnology
(Appl Biochem Biotechnol)
Vol. 194
Issue 11
Pg. 5151-5166
(Nov 2022)
ISSN: 1559-0291 [Electronic] United States |
PMID | 35699802
(Publication Type: Journal Article)
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Copyright | © 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. |
Chemical References |
- RNA, Circular
- Lipopolysaccharides
- Interleukin-10
- Tumor Necrosis Factor-alpha
- Interleukin-6
- MicroRNAs
- NF-kappa B
- Cytokines
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Topics |
- Rats
- Animals
- RNA, Circular
(genetics)
- Lipopolysaccharides
(pharmacology)
- Interleukin-10
- Tumor Necrosis Factor-alpha
- Interleukin-6
- MicroRNAs
(genetics, metabolism)
- NF-kappa B
- Spinal Cord Injuries
(genetics, metabolism)
- Apoptosis
(genetics)
- Inflammation
(genetics, metabolism)
- Cytokines
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