MicroRNA-149 Suppresses Inflammation in Nucleus Pulposus Cells of Intervertebral Discs by Regulating MyD88

BACKGROUND Intervertebral disc degeneration (IDD) is associated with low back and neck pain, but the mechanisms underlying its pathogenesis are unclear. In this study, we explored the function of microRNA-149 (miR-149) in inflammatory response mediated by lipopolysaccharide (LPS) in nucleus pulposus...

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Bibliographic Details
Published in:Medical science monitor 2019-07, Vol.25, p.4892-4900
Main Authors: Qin, Chuqiang, Lv, Yuming, Zhao, Hongpu, Yang, Bo, Zhang, Ping
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Cytokines - metabolism
Extracellular Matrix - metabolism
Intervertebral Disc - metabolism
Intervertebral Disc - pathology
Intervertebral Disc Degeneration - genetics
Intervertebral Disc Degeneration - metabolism
Intervertebral Disc Degeneration - pathology
Lab/In Vitro Research
Lipopolysaccharides - metabolism
MicroRNAs - biosynthesis
MicroRNAs - genetics
Myeloid Differentiation Factor 88 - genetics
Myeloid Differentiation Factor 88 - metabolism
Nucleus Pulposus - metabolism
Nucleus Pulposus - pathology
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
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Summary:BACKGROUND Intervertebral disc degeneration (IDD) is associated with low back and neck pain, but the mechanisms underlying its pathogenesis are unclear. In this study, we explored the function of microRNA-149 (miR-149) in inflammatory response mediated by lipopolysaccharide (LPS) in nucleus pulposus (NP) cells. MATERIAL AND METHODS Quantitative real-time PCR was used to detect miRNA and mRNA levels, while Western blotting was utilized to determine protein levels. ELISA was used to examine chemokine production. The correlation between miR-149 and MyD88 was assessed by reporter assay. Apoptosis was examined by flow cytometry. RESULTS miR-149 expression was significantly decreased after LPS exposure in NP cells. Overexpression of miR-149 reversed LPS-induced inhibition in aggrecan and collagen II expression and attenuated LPS-mediated promotion in the levels of MMP3, ADAMTS4, and inflammatory cytokines. Moreover, we found that miR-149 exerted its function by targeting MyD88 in NP cells. CONCLUSIONS miR-149 can inhibit the inflammatory response mediated by LPS in NP cells, and might be a potential target for the treatment of IDD.
ISSN:1643-3750
1234-1010
1643-3750
DOI:10.12659/MSM.915858