Ultrastructure of the Human Interspinous Ligament and Ligamentum Flavum A Preliminary Study

LEE

The Journal of Bone and Joint Surgery-American Volume

et al. 2005

Section: Methodsmentioning

confidence: 99%

Hypertrophy of Ligamentum Flavum in Lumbar Spinal Stenosis Associated With Increased Proteinase Inhibitor Concentration

LEE

The Journal of Bone and Joint Surgery-American Volume

et al. 2005

“…The CLs, which encase facet joints, have an increasing percentage of elastin posteriorly near the LF [10]. The LF, the most elastic tissue in the human body, attaches at adjacent laminae bilaterally and consists of approximately 80% elastin and 20% collagen [11,12]. The ISL, not present in all adult cervical spines, is composed of approximately 5% to 20% elastin [5,13].…”

Section: Introductionmentioning

confidence: 99%

Dynamic mechanical properties of intact human cervical spine ligaments

et al. 2007

“…28,35,48 This elastin-rich tissue is hypertrophied by aging or pathological degeneration. LF hypertrophy exacerbates the tightness of the spinal canals in patients with spinal stenosis and can be partially responsible for sciatica in these patients.…”

Section: Discussionmentioning

confidence: 99%

Expression of matrix metalloproteinase−2 and −9 in human ligamentum flavum cells treated with tumor necrosis factor−α and interleukin-1β

Kim

Hur

Park³

et al. 2016

SPI

OBJECT An in vitro study was performed to understand the potential roles of matrix metalloproteinase (MMP)-2 and MMP-9 in the elastin degradation of human ligamentum flavum (LF) cells via treatment with tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β). Previous studies have identified a decreased elastin to collagen ratio in hypertrophic LF. Among the extracellular matrix remodeling endopeptidases, MMP-2 and MMP-9 are known to have elastolytic activity. The hypothesis that activated LF cells exposed to inflammation would secrete MMP-2 and MMP-9, thereby resulting in elastin degradation, was examined. METHODS To examine MMP-2 and MMP-9 expression in human LF, cells were isolated and cultured from LF tissues that were obtained during lumbar disc surgery. Isolated LF cells were equally divided into 3 flasks and subcultured. Upon cellular confluency, the LF cells were treated with TNFα, IL-1β, or none (as a control) and incubated for 48 hours. The conditioned media were collected and assayed for MMP-2 and MMP-9 using gelatin zymography and Western blot analysis. The electrophoresis bands were compared on densitometric scans using ImageJ software. RESULTS The conditioned media from the isolated human LF cells naturally expressed 72-kD and 92-kD gelatinolytic activities on gelatin zymography. The IL-1β-treated LF cells presented sustained increases in the proenzyme/zymogen forms of MMP−2 and −9 (proMMP-2 and proMMP-9), and activeMMP-9 expression (p = 0.001, 0.022, and 0.036, respectively); the TNFα-treated LF cells showed the most elevated proMMP9 secretion (p = 0.006), as determined by Western blot analyses. ActiveMMP-2 expression was not observed on zymography or the Western blot analysis. CONCLUSIONS TNFα and IL-1β promote proMMP-2 and proMMP-9 secretion. IL-1β appears to activate proMMP-9 in human LF cells. Based on these findings, selective MMP-9 blockers or antiinflammatory drugs could be potential treatment options for LF hypertrophy.