p38 Mitogen-Activated Protein Kinase Is Involved in Interleukin-6 Secretion from Human Ligamentum Flavum–Derived Cells Stimulated by Tumor Necrosis Factor-α
- Author:
Kiyoshi YAGI
1
;
Yuta GOTO
;
Kenji KATO
;
Nobuyuki SUZUKI
;
Akira KONDO
;
Yuya WASEDA
;
Jun MIZUTANI
;
Yohei KAWAGUCHI
;
Yuji JOYO
;
Yuko WAGURI-NAGAYA
;
Hideki MURAKAMI
Author Information
- Publication Type:Basic Study
- From:Asian Spine Journal 2021;15(6):713-720
- CountryRepublic of Korea
- Language:English
-
Abstract:
Methods:HFCs were obtained from patients with LSS who underwent surgery. HFCs were stimulated by tumor necrosis factor-α (TNF-α) and a p38 MAP kinase inhibitor, SB203580. Phosphorylation of the p38 MAP kinase was analyzed by western blotting. The concentration of interleukin-6 (IL-6) in the conditioned medium was measured by enzyme-linked immunoassay and IL-6 messenger RNA expression levels were determined by real-time polymerase chain reaction.
Results:TNF-α induced the phosphorylation of p38 MAP kinase in a time-dependent manner, which was suppressed by the p38 MAP kinase inhibitor, SB203580. TNF-α also stimulated IL-6 release in both a time- and dose-dependent manner. On its own, SB203580 did not stimulate IL-6 secretion from HFCs; however, it dramatically suppressed the degree of IL-6 release stimulated by TNF-α from HFCs.
Conclusions:This is the first report suggesting that TNF-α stimulates the gene expression and protein secretion of IL-6 via p38 MAP kinase in HFCs. A noted association between tissue hypertrophy and inflammation suggests that the p38 MAP kinase inflammatory pathway may be a therapeutic molecular target for LSS.
