L Cui1, H Wei, Z-M Li, X-B Dong, P-Y Wang. 1. Department of Surgery, Xi'an Hospital of Traditional Chinese Medicine, Xi'an, China. wangpengyun@mail.sdufe.edu.cn.
Abstract
OBJECTIVE: Inflammation and fibrosis progress of nucleus pulposus (NP) cells participate in the pathologic changes of intervertebral disc degeneration (IDD). ANGPTL2 is well known for its angiogenesis and proinflammatory properties and transforming growth factor β1 (TGF-β1) is also responsible for tissue fibrosis. However, the role of ANGPTL2 in IDD and whether it is related to TGF-β1 remains unclear. This study aims to explore the relation of TGF-β1 and ANGPTL2 in the degenerative process of NP cells. PATIENTS AND METHODS: We isolated NP cells of NP tissues provided from the spine fracture patients. IL-1β was used to induce the NP cells degeneration. To determine the effect of TGF-β1 and ANGPTL2 on NP cell degeneration, we regulated the cellular TGF-β1 and ANGPTL2 expression by Recombinant human protein stimulation and siRNA transfection. Quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot was employed to investigate the expression of TGF-β1, ANGPTL2, IL-6, TNF-α, collagen I, and collagen III. RESULTS: TGF-β1 overexpression aggravated the ANGPTL2, IL-6, TNF-α, collagen I, and collagen III expressions of NP cells that caused by IL-1β, which was rejected by ANGPTL2 gene silencing. Besides, the silencing of TGF-β1 weakened the ANGPTL2 expression. ANGPTL2 overexpression promoted the NP cells inflammation and fibrosis via increasing IL-6, TNF-α, collagen I, and collagen III expression, which was sharpened by a consequent increase of TGF-β1 expression. CONCLUSIONS: This study, for the first time, points that TGF-β1 aggravates degenerative NP cells inflammation and fibrosis via the mediation of ANGPTL2.
OBJECTIVE:Inflammation and fibrosis progress of nucleus pulposus (NP) cells participate in the pathologic changes of intervertebral disc degeneration (IDD). ANGPTL2 is well known for its angiogenesis and proinflammatory properties and transforming growth factor β1 (TGF-β1) is also responsible for tissue fibrosis. However, the role of ANGPTL2 in IDD and whether it is related to TGF-β1 remains unclear. This study aims to explore the relation of TGF-β1 and ANGPTL2 in the degenerative process of NP cells. PATIENTS AND METHODS: We isolated NP cells of NP tissues provided from the spine fracturepatients. IL-1β was used to induce the NP cells degeneration. To determine the effect of TGF-β1 and ANGPTL2 on NP cell degeneration, we regulated the cellular TGF-β1 and ANGPTL2 expression by Recombinant human protein stimulation and siRNA transfection. Quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot was employed to investigate the expression of TGF-β1, ANGPTL2, IL-6, TNF-α, collagen I, and collagen III. RESULTS: TGF-β1 overexpression aggravated the ANGPTL2, IL-6, TNF-α, collagen I, and collagen III expressions of NP cells that caused by IL-1β, which was rejected by ANGPTL2 gene silencing. Besides, the silencing of TGF-β1 weakened the ANGPTL2 expression. ANGPTL2 overexpression promoted the NP cells inflammation and fibrosis via increasing IL-6, TNF-α, collagen I, and collagen III expression, which was sharpened by a consequent increase of TGF-β1 expression. CONCLUSIONS: This study, for the first time, points that TGF-β1 aggravates degenerative NP cells inflammation and fibrosis via the mediation of ANGPTL2.