NF-κB 1-induced LINC00665 regulates inflammation and apoptosis of neurons caused by spinal cord injury by targeting miR-34a-5p

Background: Spinal cord injury (SCI) has high disability rate and low cure rate, which frustrates the patients and brings a heavy burden to their families. This study aimed to explore whether NF-κB1 could induce the expression of LINC00665 and form a feedback loop with miR-34a-5p to regulate inflamm...

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Bibliographic Details
Published in:Neurological research (New York) 2021-05, Vol.43 (5), p.418-427
Main Authors: Deng, Qilong, Ma, Lili, Chen, Ting, Yang, Yu, Ma, Yuetao, Ma, Lizhong
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Cell Survival
Disease Models, Animal
Inflammation
LINC00665
Lipopolysaccharides - administration & dosage
Male
MicroRNAs - metabolism
miR-34a-5p
NF-kappa B - metabolism
NFKB1
PC12 Cells
Rats
RNA, Long Noncoding - metabolism
Signal Transduction
Spinal Cord Injuries - metabolism
Spinal Cord Injuries - pathology
spinal cord injury
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Summary:Background: Spinal cord injury (SCI) has high disability rate and low cure rate, which frustrates the patients and brings a heavy burden to their families. This study aimed to explore whether NF-κB1 could induce the expression of LINC00665 and form a feedback loop with miR-34a-5p to regulate inflammation and apoptosis of neurons. Results: Basso, Beattie, and Bresnahan (BBB) scoring was decreased, damage for spinal cord tissue was aggravated and neuron number was decreased in SCI rats. The levels of TNF-α, IL-1β and IL-6 in serum and the expression of LINC00665 and NF-κB1 in spinal cord tissues were all increased in SCI rats. After LPS induction, PC12 cell viability was decreased. The expression of LINC00665 and NF-κB1 in LPS-induced PC12 cells was increased, which was partially reversed by BAY11-7082 (NF-κB inhibitor). Inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation and down-regulated the NF-κB1 expression in LPS-induced PC12 cells. Furthermore, miR-34a-5p expression was decreased in LPS-induced PC12 cells, which could be promoted by inhibition of LINC00665. miR-34a-5p inhibitor restrained the effect of inhibition of LINC00665 on NF-κB1 expression in LPS-induced PC12 cells. Conclusion: inhibition of LINC00665 improved cell viability, suppressed apoptosis and inflammation in LPS-induced PC12 cells, and the NF-κB1/LINC00665/miR-34a-5ploop might be a useful therapeutic target in SCI treatment.
ISSN:0161-6412
1743-1328
DOI:10.1080/01616412.2020.1866373