Open AccessInterleukin-1β promotes interleulin-6 expression via ERK1/2 signaling pathway in canine dermal fibroblasts
Author(s) -
Nanako Kitanaka,
Rei Nakano,
Kanako Sugiura,
Taku Kitanaka,
Shinichi Namba,
Tadayoshi Konno,
Tomohiro Nakayama,
Hiroshi Saito
Publication year - 2019
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0220262
Subject(s) - mapk/erk pathway , kinase , p38 mitogen activated protein kinases , microbiology and biotechnology , proinflammatory cytokine , small interfering rna , signal transduction , cytokine , protein kinase a , mitogen activated protein kinase , biology , chemistry , transfection , inflammation , cell culture , immunology , genetics
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in the regulation of the immune response and inflammation. In this study, we investigated effect of the proinflammatory cytokine interleukin-1β (IL-1β) on IL-6 expression in canine dermal fibroblasts. IL-1β induced IL-6 mRNA expression and protein release in a time- and dose-dependent manner. When cells were treated with inhibitors of mitogen-activated protein kinases (MAPKs), the extracellular signal-regulated kinase (ERK) inhibitor FR180240 inhibited IL-1β-induced IL-6 mRNA expression, but not SP600125 or SKF86002, which are c-Jun N-terminal kinase (JNK) and p38 MAPK inhibitors, respectively. In cells treated with U0126, an inhibitor of MAPK/ERK kinase (MEK), which activates ERK, IL-1β-induced IL-6 mRNA expression was also inhibited. IL-1β stimulated ERK1/2 phosphorylation. In cells transfected with ERK1 and ERK2 isoform siRNAs, IL-1β-induced IL-6 mRNA expression was reduced. These observations suggest that IL-1β induces IL-6 expression via ERK1/2 signaling pathway in canine dermal fibroblasts.