title: Expression of the JAK/STAT signaling pathway in the ligamentum flavum of patients with lumbar spinal canal stenosis.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan. Electronic address: yamahatad3@gmail.com.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Yamahata
authors.affiliation: Department of Neurological Surgery, Aichi Medical University, Aichi, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Osuka
authors.affiliation: Department of Neurosurgery, Shinshu University, Nagano, Japan.
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Aoyama
authors.affiliation: Department of Neurological Surgery, Aichi Medical University, Aichi, Japan.
authors.forename: Muneyoshi
authors.initials: M
authors.lastname: Yasuda
authors.affiliation: Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tokimura
authors.affiliation: Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
authors.forename: Kazunori
authors.initials: K
authors.lastname: Arita
authors.affiliation: Department of Neurological Surgery, Aichi Medical University, Aichi, Japan.
authors.forename: Masakazu
authors.initials: M
authors.lastname: Takayasu
mesh_terms: D000368:Aged; D001707:Biopsy, Needle; D015153:Blotting, Western; D015331:Cohort Studies; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D053612:Janus Kinases / Q000235:genetics*; D017843:Ligamentum Flavum / Q000378:metabolism / Q000473:pathology*; D008159:Lumbar Vertebrae; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D050796:STAT3 Transcription Factor / Q000235:genetics*; D015398:Signal Transduction; D013130:Spinal Stenosis / Q000235:genetics* / Q000473:pathology; D018709:Statistics, Nonparametric
chemical_list: D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D053612:Janus Kinases