Expression of the JAK/STAT signaling pathway in the ligamentum flavum of patients with lumbar spinal canal stenosis.

Abstract

Ligamentum flavum (LF) hypertrophy is an important cause of lumbar spinal canal stenosis (LSS), one of the most common spinal disorders in the elderly. Although many cytokines are reported to be associated with LF hypertrophy, the intracellular signaling system is rarely discussed. The purpose of this study was to identify the JAK/STAT signaling pathway and to examine the role of the JAK/STAT systems in the hypertrophied LF. The LF of 10 LSS patients was analyzed and the expression of JAK1, STAT3, phosphorylated (p)-STAT3, and actin was examined by Western blot analysis. The expression of p-STAT3 was also examined by immunostaining and its positive cell ratio was compared between LSS and non-LSS samples. We measured the thickness of the LF on magnetic resonance images and studied the relationship between its thickness and the expression of p-STAT3. JAK1, STAT3, and p-STAT3 were detected in almost all samples by Western blot analysis. Immunoreactivity against p-STAT3 was observed mainly in endothelial- and fibroblast-like cells. The expression of p-STAT3 was significantly higher in LSS than non-LSS samples; it was significantly stronger on the dorsal than the dural side of the LF and positively correlated with the thickness of the LF on the dorsal side. The JAK/STAT signaling pathway is positively correlated with the thickness of the LF. Our findings suggest that JAK1 and STAT3 molecules are involved in and regulate LF hypertrophy.