Abstract
BackgroundIntervertebral disk degeneration (IDD) is caused by nucleus pulposus (NP) degeneration and extracellular matrix (ECM) remodeling and cartilage intermediate layer protein (CILP) expression has been confirmed to be increased in IDD. This study is mainly conducted to clarify the mechanism of CILP in the NP cell degeneration and ECM remodeling in IDD.MethodsCILP expression in the degenerated NP tissues and cells is quantified by quantitative real-time PCR and western blot. CILP function is assessed by cell cycle assay, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry, β-galactosidase staining, and the detection of ECM-related molecules aggrecan, collagen type I, collagen type II, MMP-3, and MMP-9 expression is accomplished by qRT-PCR. The potential mechanism is authenticated by dual-luciferase reporter gene assay.ResultsCILP was increased in the degenerated NP tissues and cells, and the knockdown of CILP promoted the NP cell cycle, increased cell activity, and repressed cell apoptosis and repressed cell senescence and ECM production. Moreover, miR-330-5p targeted the CILP 3′-untranslated region, and miR-330-5p negatively regulated CILP expression. Moreover, the overexpression of miR-330-5p repressed NP cell degeneration and ECM remodeling to relieve IDD by downregulating CILP.ConclusionMiR-330-5p represses NP cell degeneration and ECM remodeling to ameliorate IDD by downregulating CILP.
Highlights
Low back pain is a worldwide challenge that poses a serious threat to the physical and mental health of humans and imposes a burden on the social economy [1, 2]
Li et al Journal of Orthopaedic Surgery and Research (2021) 16:440 upregulated in the degenerated nucleus pulposus (NP) tissues and cells, and we further proved that the knockdown of cartilage intermediate layer protein (CILP) repressed NP cell degeneration and extracellular matrix (ECM) remodeling
CILP is upregulated in the degenerated NP tissues and cells accumulating evidence authenticates that CILP has a regulatory function in various human diseases [11, 12], the function of CILP in the progression of Intervertebral disk degeneration (IDD) has not been fully elucidated
Summary
Low back pain is a worldwide challenge that poses a serious threat to the physical and mental health of humans and imposes a burden on the social economy [1, 2]. Low back pain is mainly caused by intervertebral disk degeneration (IDD) [3]. IDD is caused by multiple factors, among which the degeneration of the nucleus pulposus (NP) and the remodeling of extracellular matrix (ECM) are the main factors for the acceleration of the development of IDD [4, 5]. The in-depth exploration of Cartilage intermediate layer protein (CILP) encodes cartilage intermediate layer protein and it has been corroborated that the abnormal expression of CILP is associated with a variety of human diseases [6, 7]. Intervertebral disk degeneration (IDD) is caused by nucleus pulposus (NP) degeneration and extracellular matrix (ECM) remodeling and cartilage intermediate layer protein (CILP) expression has been confirmed to be increased in IDD.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
