The content of lactic acid gradually increased after annular lesion, associated with the damage of AF structural and the decrease of Col -II and aggrecan in NP tissue, which leading to the disc degeneration.
The in vivo experiments showed that the HIF-2α controlled the catabolic factors MMP-13 and ADAMTS-4 that regulated the collagen II and aggrecan metabolism in disc degeneration.
Polymorphisms in several structural and inflammatory genes like collagens, aggrecan, matrix metalloproteinases are associated with the risk of disc degeneration.
An in vitro model of disc degeneration using human nucleus pulposus cells (hNPCs) and ex vivo culture of mouse intervertebral discs organs under the actions of inflammatory cytokines were used, and the expression of Col II and aggrecan in hNPCs were detected by semi-quantitative western blot analysis, and the mRNA expression of the genes than encode Col II and aggrecan were detected by reverse transcription‑quantitative polymerase chain reaction (RT-qPCR).
A systematic review of the relationship between the distributions of aggrecan gene VNTR polymorphism and degenerative disc disease/osteoarthritis.<i>Bone Joint Res</i> 2018;7:308-317.
Histology and immunostaining revealed that disc degeneration was not significantly different between the OVX + NS rats and the OVX + PTH rats, compared with the Sham group; the structure of nucleus pulposus was disordered, the expression of collagen I was increased, and collagen II and aggrecan were decreased.
The stable expression of <i>CTGF</i> and <i>TIMP1</i> genes <i>in vivo</i> promoted the synthesis of aggrecan and type II collagen in the nucleus pulposus in the rhesus monkey model of intervertebral disc degeneration, which has a potential for intervertebral disc regeneration.
Therefore, our study shows that HIF-1α regulates collagen Π and aggrecan expression through NOTCH1 signaling and implicate NOTCH1 as a potential therapeutic target in disc degeneration.
Our study provides evidence that COL2A1 and Aggrecan genetic polymorphisms may be correlated with the risk and clinicopathological features of IVDD in a Chinese Han population, and ACGL and GTCL haplotypes may be protective factors of IVDD.
Genetic polymorphisms in 20 genes have been analyzed in association with DD, including vitamin D receptor, growth differentiation factor 5 (GDF5), aggrecan, collagen Types I, IX, and XI, fibronectin, hyaluronan and proteoglycan link protein 1 (HAPLN1), thrombospondin, cartilage intermediate layer protein (CILP), asporin, MMP1, 2, and 3, parkinson protein 2, E3 ubiquitin protein ligase (PARK2), proteosome subunit β type 9 (PSMB9), tissue inhibitor of metalloproteinase (TIMP), cyclooxygenase-2 (COX2), and IL1α, IL1β, and IL6.
Intervertebral disc degeneration (IDD) pertains to the loss of extracellular matrix (ECM), particularly the early loss of aggrecan, the turnover of which is regulated by ADAMTSs.
We wanted to investigate the patterns of the variable numbers of tandem repeat polymorphism in the aggrecan CS1 domain of Koreans, and we analyzed the association between the polymorphism and intervertebral disc degeneration.
Aggrecan fragments have been found in human degenerated discs, and an association between the aggrecan VNTR polymorphism and intervertebral disc degeneration has been previously reported in middle-aged Finnish men.
Our data suggest that carrying shorter AGC1 alleles with less than 24 repeats could predispose a subject to lumbar disk degeneration disease in northern Iran.
However, the interaction between aggrecan gene VNTR polymorphism and smoking in symptomatic intervertebral disc degeneration (IDD) has not been well studied.
To determine the expression of ADAMTS-4, a metalloproteinase capable of digesting aggrecan, and its role in herniated lumbar intervertebral disc degradation.
Tryptophan alleles in COL9A2 and COL9A3 have been shown to be associated with lumbar disc disease in the Finnish population, and polymorphisms in the vitamin D receptor gene (VDR) (FokI and TaqI), the matrix metalloproteinase-3 gene (MMP-3) and an aggrecan gene (AGC1) VNTR have been reported to be associated with disc degeneration.