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  • Title: Poly(I:C)-induced adhesion molecule expression mediated by NF-{kappa}B and phosphoinositide 3-kinase-Akt signaling pathways in human corneal fibroblasts.
    Author: Orita T, Kimura K, Zhou HY, Nishida T.
    Journal: Invest Ophthalmol Vis Sci; 2010 Nov; 51(11):5556-60. PubMed ID: 20574012.
    Abstract:
    PURPOSE: Viral infection at the ocular surface can lead to the chronic condition of viral stromal keratitis. Polyinosinic-polycytidylic acid [poly(I:C)], an analog of viral double-stranded RNA, induces the expression of adhesion molecules in cultured corneal fibroblasts. The authors investigated the roles of nuclear factor (NF)-κB and phosphoinositide 3-kinase (PI3K)-Akt signaling pathways in the poly(I:C)-induced expression of adhesion molecules in corneal fibroblasts. METHODS: Human corneal fibroblasts were cultured with poly(I:C) in the absence or presence of IκB kinase 2 (IKK2) inhibitor (an inhibitor of NF-κB activation) or the PI3K inhibitor LY294002. The expression of vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, ICAM-2, and E-selectin, as well as the phosphorylation of the NF-κB inhibitory protein IκB-α and Akt, were examined by immunoblot analysis. The subcellular localization of adhesion molecules was determined by immunofluorescence analysis. RESULTS: Poly(I:C) increased the expression of VCAM-1 and ICAM-1 but not that of ICAM-2 or E-selectin in corneal fibroblasts. Poly(I:C) also induced the phosphorylation of IκB-α and Akt. The poly(I:C)-induced expression of VCAM-1 and ICAM-1 was attenuated by both IKK2 inhibitor and LY294002. CONCLUSIONS: The NF-κB and PI3K-Akt signaling pathways mediate the poly(I:C)-induced upregulation of VCAM-1 and ICAM-1 in corneal fibroblasts, with PI3K acting upstream of NF-κB activation. These pathways thus likely modulate local immune and inflammatory responses to viral infection in the corneal stroma.
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