Conclusion
SPARC was detected in human LF and significantly upregulated in the clinical samples of hypertrophic LF compared to their normal counterparts. We also demonstrated an increased level of SPARC in an in vitro fibrosis model of LF. Thus, SPARC could be a crucial biomarker for the pathogenesis of hypertrophic LF and a therapeutic target for LSS.
Methods
Hypertrophic LF samples were obtained from 8 patients with L4/5 lumbar spinal stenosis (LSS) during the decompressive laminectomy. Non-hypertrophic LF from age- and sex-matched 8 patients with L4/5 lumbar disc herniation was selected as control. An in vitro model of fibrosis in human LF cells was established by interleukin 6 (IL-6) to assess SPARC expression.
Results
Hypertrophic LF samples had higher fibrosis scores than control samples by Masson's trichrome staining (3.6 vs. 1.3, P < .001). Hypertrophic LF samples had significantly more positive staining for collagen and SPARC. Collagen III (Col3), α smooth muscle actin (α-SMA), and SPARC mRNA expression levels were significantly higher in hypertrophic LF samples than in control samples by qPCR. SPARC expression and fibrotic and inflammatory makers (collagen I, Col3, IL-6, interleukin 1β) were significantly upregulated in IL-6 stimulation of normal LF in vitro.