Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation

Abstract Epidemiological studies have concluded that hyperlipidemia and atherosclerosis were related to intervertebral disc degeneration (IVDD). The presence of oxidized low density lipoprotein (ox-LDL) and the expression of lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) have not be...

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Autores principales:	Xinhua Li, Xuejun Wang, Zhouyang Hu, Zhaoxiong Chen, Haoxi Li, Xiaoming Liu, Zhi Yao Yong, Shanjing Wang, Zhanying Wei, Yingchao Han, Jun Tan, Cong Li, Xiao bo He, Guixin Sun, Desheng Wu, Lijun Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4037d2bac8f642da951de0bac25557fc
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spelling	oai:doaj.org-article:4037d2bac8f642da951de0bac25557fc2021-12-02T16:06:06ZPossible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation10.1038/s41598-017-07780-x2045-2322https://doaj.org/article/4037d2bac8f642da951de0bac25557fc2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07780-xhttps://doaj.org/toc/2045-2322Abstract Epidemiological studies have concluded that hyperlipidemia and atherosclerosis were related to intervertebral disc degeneration (IVDD). The presence of oxidized low density lipoprotein (ox-LDL) and the expression of lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) have not been explored in this tissue. In this study, we investigated the presence of ox-LDL and the expression of its receptor LOX-1 in non-degenerated, degenerated or herniated human intervertebral discs (IVDs). The expression of LOX-1 and matrix metalloproteinase 3 (MMP3) were studied after incubating nucleus pulposus cells (NPCs) with ox-LDL. The presence of ox-LDL and LOX-1 was positively related with the extent of IVDD in nucleus pulposus (NP), end-plate cartilage and outer annulus fibrous, but not with the extent of degeneration of inter annulus fibrous. Ox-LDL significantly reduced the viability of human NPCs in a dose and time-dependent manner, and increased the expression of MMP3 induced by LOX-1. Pretreatment with anti-human LOX-1 monoclonal antibody reversed these effects. Ox-LDL, principally mediated by LOX-1, enhanced MMP3 production in NPCs through the NF-κB signaling pathway. In conclusion, increased accumulation of ox-LDL and LOX-1 in IVDs indicates a specific role of the receptor-ligand interaction in degeneration or herniation of IVDs.Xinhua LiXuejun WangZhouyang HuZhaoxiong ChenHaoxi LiXiaoming LiuZhi Yao YongShanjing WangZhanying WeiYingchao HanJun TanCong LiXiao bo HeGuixin SunDesheng WuLijun LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xinhua Li Xuejun Wang Zhouyang Hu Zhaoxiong Chen Haoxi Li Xiaoming Liu Zhi Yao Yong Shanjing Wang Zhanying Wei Yingchao Han Jun Tan Cong Li Xiao bo He Guixin Sun Desheng Wu Lijun Li Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
description	Abstract Epidemiological studies have concluded that hyperlipidemia and atherosclerosis were related to intervertebral disc degeneration (IVDD). The presence of oxidized low density lipoprotein (ox-LDL) and the expression of lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) have not been explored in this tissue. In this study, we investigated the presence of ox-LDL and the expression of its receptor LOX-1 in non-degenerated, degenerated or herniated human intervertebral discs (IVDs). The expression of LOX-1 and matrix metalloproteinase 3 (MMP3) were studied after incubating nucleus pulposus cells (NPCs) with ox-LDL. The presence of ox-LDL and LOX-1 was positively related with the extent of IVDD in nucleus pulposus (NP), end-plate cartilage and outer annulus fibrous, but not with the extent of degeneration of inter annulus fibrous. Ox-LDL significantly reduced the viability of human NPCs in a dose and time-dependent manner, and increased the expression of MMP3 induced by LOX-1. Pretreatment with anti-human LOX-1 monoclonal antibody reversed these effects. Ox-LDL, principally mediated by LOX-1, enhanced MMP3 production in NPCs through the NF-κB signaling pathway. In conclusion, increased accumulation of ox-LDL and LOX-1 in IVDs indicates a specific role of the receptor-ligand interaction in degeneration or herniation of IVDs.
format	article
author	Xinhua Li Xuejun Wang Zhouyang Hu Zhaoxiong Chen Haoxi Li Xiaoming Liu Zhi Yao Yong Shanjing Wang Zhanying Wei Yingchao Han Jun Tan Cong Li Xiao bo He Guixin Sun Desheng Wu Lijun Li
author_facet	Xinhua Li Xuejun Wang Zhouyang Hu Zhaoxiong Chen Haoxi Li Xiaoming Liu Zhi Yao Yong Shanjing Wang Zhanying Wei Yingchao Han Jun Tan Cong Li Xiao bo He Guixin Sun Desheng Wu Lijun Li
author_sort	Xinhua Li
title	Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
title_short	Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
title_full	Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
title_fullStr	Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
title_full_unstemmed	Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
title_sort	possible involvement of the oxldl/lox-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/4037d2bac8f642da951de0bac25557fc
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Possible involvement of the oxLDL/LOX-1 system in the pathogenesis and progression of human intervertebral disc degeneration or herniation

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