Expression of phosphoinositide-specific phospholipase C isoenzymes in cultured astrocytes activated after stimulation with lipopolysaccharide

✍ Scribed by Vincenza Rita Lo Vasco; Cinzia Fabrizi; Lorenzo Fumagalli; L. Cocco

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 182 KB
• Volume: 109
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.22480

✦ Synopsis

Abstract

Signal transduction pathways, involved in cell cycle and activities, depend on various components including lipid signalling molecules, such as phosphoinositides and related enzymes. Many evidences support the hypothesis that inositol lipid cycle is involved in astrocytes activation during neurodegeneration. Previous studies investigated the pattern of expression of phosphoinositide‐specific phospholipase C (PI‐PLC) family isoforms in astrocytes, individuating in cultured neonatal rat astrocytes, supposed to be quiescent cells, the absence of some isoforms, accordingly to their well known tissue specificity. The same study was conducted in cultured rat astrocytoma C6 cells and designed a different pattern of expression of PI‐PLCs in the neoplastic counterpart, accordingly to literature suggesting a PI signalling involvement in tumour progression. It is not clear the role of PI‐PLC isoforms in inflammation; recent data demonstrate they are involved in cytokines production, with special regard to IL‐6. PI‐PLCs expression in LPS treated neonatal rat astrocytes performed by using RT‐PCR, observed at 3, 6, 18 and 24 h intervals, expressed: PI‐PLC beta1, beta4 and gamma1 in all intervals analysed; PI‐PLC delta1 at 6, 18 and 24 h; PI‐PLC delta3 at 6 h after treatment. PI‐PLC beta3, delta4 and epsilon, present in untreated astrocytes, were not detected after LPS treatment. Immunocytochemical analysis, performed to visualize the sub‐cellular distribution of the expressed isoforms, demonstrated different patterns of localisation at different times of exposure. These observations suggest that PI‐PLCs expression and distribution may play a role in ongoing inflammation process of CNS. J. Cell. Biochem. 109: 1006–1012, 2010. © 2010 Wiley‐Liss, Inc.