Abstract
Hypertrophy of ligamentum flavum (LF) contributes to lumbar spinal stenosis (LSS) and is caused mainly by fibrosis. Recent data indicate that miR-155 plays a crucial role in the pathogenesis of different fibrotic diseases. This study aimed to test the hypothesis that miR-155 exerts effects on LF thickness by regulating collagen expression. We found that LF thickness and the expression of collagen I and, collagen III were higher in LF from LSS patients than in LF from lumbar disc herniation (LDH) patients (P < 0.01). The expression of miR-155 was significantly higher in LF from LSS group than in LF from LDH group (P < 0.01). miR-155 level was positively correlated with LF thickness (r = 0.958, P < 0.01), type I collagen level (r = 0.825, P < 0.01), and type III collagen level (r = 0.827, P < 0.01). miR-155 mimic increased mRNA and protein expression of collagen I and collagen III in fibroblasts isolated from LF, while miR-155 sponge decreased mRNA and protein expression of collagen I and III in fibroblasts. In conclusions, miR-155 is a fibrosis-associated miRNA and may play important role in the pathogenesis of LF hypertrophy.
Highlights
IntroductionLumbar spinal stenosis (LSS) is defined as the narrowing of the spinal canal with cord or nerve root impingement which results in the symptoms of radiculopathy or pseudoclaudication [1]
Lumbar spinal stenosis (LSS) is a common condition in elderly patients
Histological analysis showed that the elastic fiber area decreased and collagen area increased in ligamentum flavum (LF) from LSS group, compared to lumbar disc herniation (LDH) group
Summary
LSS is defined as the narrowing of the spinal canal with cord or nerve root impingement which results in the symptoms of radiculopathy or pseudoclaudication [1]. Hypertrophy of the ligamentum flavum (LF) is usually involved in the pathogenesis of LSS, which can reduce the diameter of the spinal canal and compress the dural sac and nerve roots, resulting in symptoms, even in the absence of a bulging annulus fibrosus or herniated nucleus pulposus or osseous spurs [2,3,4]. LF is a well-defined elastic structure that consists of elastic (80%) and collagen (20%) fibers [5]. Hypertrophied LF tissues become disorganized and show decreased levels and degeneration of elastic fibers but increased levels of collagen fibers [6, 7]. During LF hypertrophy, there are increases in the expression and activity of various molecules, including matrix metalloproteases (MMPs) [8,9,10], tissue inhibitors of matrix metalloproteases (TIMPs) [11], platelet-derived growth factor-BB (PDGF-BB) [12], connective tissue growth factor (CTGF) [13], bone morphogenetic protein (BMP) [14], and inflammatory cytokines [15,16,17]
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