Purchase this article with an account.
Tomoko Orita, Kazuhiro Kimura, Koh-Hei Sonoda; Role of the JNK Signaling Pathway in Down-Regulation of Connexin43 by TNF-α in Human Corneal Fibroblasts. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1096.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Corneal fibroblasts are connected to each other via gap junctions and contribute to corneal homeostasis. We previously showed that Tumor necrosis factor (TNF)-α, a proinflammatory cytokine, down-regulates connexin43 (Cx43), gap junctional protein, and then inhibits gap-junctional intercellular communication (GJIC) in corneal fibroblasts. The authors examined the role of MAPK signaling pathway in the TNF-α-induced down-regulation of Cx43 in these cells.
Cultured corneal fibroblasts were exposed to TNF-α in the absence or presence of inhibitors of mitogen-activated protein kinase (MAPK) signaling pathways.
The effects of TNF-α on Cx43 expression were attenuated by an inhibitor of c-Jun NH2-terminal kinase (JNK inhibitor II) but not by inhibitors of signaling by extracellular signal-regulated kinase (PD98059) or by p38 MAPK (SB203580). JNK inhibitor II also attenuated the inhibitory effect of TNF-α on GJIC and distribution of Cx43.
The inhibitory effects of TNF-α on Cx43 expression and GJIC are mediated, at least in part, by the JNK signaling pathway. JNK signaling pathway in corneal fibroblasts may play an important role in corneal inflammation.
This PDF is available to Subscribers Only