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. 2010 Jul 9;5(7):e11512. doi: 10.1371/journal.pone.0011512

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Benakanakere et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Triggering TLRs by respective ligand stimulates the cells to induce HBD-2. This induction can be ablated by a pharmacological inhibitor against Sphk-1, and inhibition of GSK3 by SB216763 or siGSK3-β in the absence of Sphk-1 inhibition can augment HBD-2 secretion. Inhibition of PI3K by either wortmannin or LY294002 abrogated HBD-2 in gingival epithelial cells. PI3K activated Akt, the phosphorylation of Akt inhibited GSK3 in turn activating ERK 1/2. ERK 1/2 activates Sphk-1 by phosphorylation at Ser225 and increase NF-kB activity. This show PI3K-Akt-GSK3-ERK1/2-Sphk-1 mediates HBD-2 synthesis in gingival epithelial cells.