Tags

Type your tag names separated by a space and hit enter

Overexpression of miR-140-5p inhibits lipopolysaccharide-induced human intervertebral disc inflammation and degeneration by downregulating toll-like receptor 4.
Oncol Rep. 2018 Aug; 40(2):793-802.OR

Abstract

Toll-like receptor 4 (TLR4) families are receptors for ligands that initiate extracellular or intracellular signaling, such as lipopolysaccharides (LPS). It has been reported that TLR4 activation resulted in the upregulation of a coordinated set of proinflammatory mediators and inhibition of matrix expression in the intervertebral disc (IVD). miR-140-5p (miR-140) is reported to participate in cellular anti-inflammatory processes and target TLR4. In the present study, we investigated the relationship between TLR4 and miR-140 in IVD degeneration. The expression of TLR4, interleukin (IL)-6, IL-I, L-1β and tumor necrosis factor (TNF)-α was higher, in high-grade IVD degeneration tissues than in low-grade tissues. In contrast, the expression of miR-140, aggrecan and collagen type II was lower in high-grade IVD degeneration tissues than in low-grade IVD degeneration tissues. LPS stimulation resulted in significant increases in TLR4 expression and decreases in miR-140 expression in nucleus pulposus (NP) cells and TLR4 was identified as a target of miR-140 by dual-luciferase reporter assay. The overexpression of miR-140 inhibited the upregulation of the expression of TLR4, TNF-α, IL-1β and IL-6 inflammation cytokines, and the activation of NF-κB and reversed the downregulation of the expression of aggrecan and collagen type II induced by LPS stimulation. In conclusion, the present study may lead to a greater understanding of IVD degeneration and provide new insights into the treatment of this disease.

Authors+Show Affiliations

Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.Department of Orthopaedics, The Affiliated Changzhou No. 2 People's Hospital with Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29901170

Citation

Zhang, Qiang, et al. "Overexpression of miR-140-5p Inhibits Lipopolysaccharide-induced Human Intervertebral Disc Inflammation and Degeneration By Downregulating Toll-like Receptor 4." Oncology Reports, vol. 40, no. 2, 2018, pp. 793-802.
Zhang Q, Weng Y, Jiang Y, et al. Overexpression of miR-140-5p inhibits lipopolysaccharide-induced human intervertebral disc inflammation and degeneration by downregulating toll-like receptor 4. Oncol Rep. 2018;40(2):793-802.
Zhang, Q., Weng, Y., Jiang, Y., Zhao, S., Zhou, D., & Xu, N. (2018). Overexpression of miR-140-5p inhibits lipopolysaccharide-induced human intervertebral disc inflammation and degeneration by downregulating toll-like receptor 4. Oncology Reports, 40(2), 793-802. https://doi.org/10.3892/or.2018.6488
Zhang Q, et al. Overexpression of miR-140-5p Inhibits Lipopolysaccharide-induced Human Intervertebral Disc Inflammation and Degeneration By Downregulating Toll-like Receptor 4. Oncol Rep. 2018;40(2):793-802. PubMed PMID: 29901170.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overexpression of miR-140-5p inhibits lipopolysaccharide-induced human intervertebral disc inflammation and degeneration by downregulating toll-like receptor 4. AU - Zhang,Qiang, AU - Weng,Yiping, AU - Jiang,Yuqing, AU - Zhao,Shujie, AU - Zhou,Dong, AU - Xu,Nanwei, Y1 - 2018/06/12/ PY - 2017/09/15/received PY - 2018/04/20/accepted PY - 2018/6/15/pubmed PY - 2018/10/18/medline PY - 2018/6/15/entrez SP - 793 EP - 802 JF - Oncology reports JO - Oncol. Rep. VL - 40 IS - 2 N2 - Toll-like receptor 4 (TLR4) families are receptors for ligands that initiate extracellular or intracellular signaling, such as lipopolysaccharides (LPS). It has been reported that TLR4 activation resulted in the upregulation of a coordinated set of proinflammatory mediators and inhibition of matrix expression in the intervertebral disc (IVD). miR-140-5p (miR-140) is reported to participate in cellular anti-inflammatory processes and target TLR4. In the present study, we investigated the relationship between TLR4 and miR-140 in IVD degeneration. The expression of TLR4, interleukin (IL)-6, IL-I, L-1β and tumor necrosis factor (TNF)-α was higher, in high-grade IVD degeneration tissues than in low-grade tissues. In contrast, the expression of miR-140, aggrecan and collagen type II was lower in high-grade IVD degeneration tissues than in low-grade IVD degeneration tissues. LPS stimulation resulted in significant increases in TLR4 expression and decreases in miR-140 expression in nucleus pulposus (NP) cells and TLR4 was identified as a target of miR-140 by dual-luciferase reporter assay. The overexpression of miR-140 inhibited the upregulation of the expression of TLR4, TNF-α, IL-1β and IL-6 inflammation cytokines, and the activation of NF-κB and reversed the downregulation of the expression of aggrecan and collagen type II induced by LPS stimulation. In conclusion, the present study may lead to a greater understanding of IVD degeneration and provide new insights into the treatment of this disease. SN - 1791-2431 UR - https://www.unboundmedicine.com/medline/citation/29901170/Overexpression_of_miR_140_5p_inhibits_lipopolysaccharide_induced_human_intervertebral_disc_inflammation_and_degeneration_by_downregulating_toll_like_receptor_4_ L2 - http://www.spandidos-publications.com/or/40/2/793 DB - PRIME DP - Unbound Medicine ER -