Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2], mainly produced by the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5KI) family members, PIP5KIα, PIP5KIβ and PIP5KIγ, is an important regulator of diverse cellular processes at the cell surface, such as cell survival, cell proliferation, phagocytosis, macropinocytosis membraned ruffles, ion channels transporters, cytoskeletal regulation and intracellular vesicle trafficking. Recently, it was reported that PI(4,5)P2 was important for neurodegenerative diseases. Nevertheless, expression and regulatory role of PIP5KIs in rat primary glia cell remain poorly understood. This present study has shown that PIP5KIα and PIP5KIγ are significantly upregulated in response to ganglioside mixture (Gmix) and lipopolysaccharide that are well known inflammatory stimulators. c-Jun N-terminal Kinase, phosphoinositide 3-kinase/Akt and extracellular signal-regulated kinase signaling pathways were responsible for the upregulation of PIP5KIα and PIP5KIγ. In addition, we have examined whether gene knockdown of PIP5KIα plays a role in the nuclear factor kappa B (NF-κB) signaling pathway. We found that PIP5KIα knockdown could inhibit the phosphorylation of NF-κB p65 in response to Gmix, leading to decrease in Gmix-induced proinflammatory cytokines, tumor necrosis factor α and interleukin-1β.These results suggest that PIP5KIα may act as a regulator of brain inflammation by modulating NF-κB signaling.
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