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Expression pattern and sub‐cellular distribution of phosphoinositide specific phospholipase C enzymes after treatment with U‐73122 in rat astrocytoma cells
Author(s) -
Lo Vasco Vincenza Rita,
Fabrizi Cinzia,
Panetta Barbara,
Fumagalli Lorenzo,
Cocco Lucio
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22614
Subject(s) - phospholipase c , inositol , phosphoinositide phospholipase c , signal transduction , biology , gene isoform , gq alpha subunit , microbiology and biotechnology , cell culture , phospholipase , phospholipase a2 , biochemistry , receptor , enzyme , g protein , gene , genetics
Phosphoinositide specific phospholipase C (PI‐PLC) enzymes interfere with the metabolism of inositol phospholipids (PI), molecules involved in signal transduction, a complex process depending on various components. Many evidences support the hypothesis that, in the glia, isoforms of PI‐PLC family display different expression and/or sub cellular distribution under non‐physiological conditions such as the rat astrocytes activation during neurodegeneration, the tumoural progression of some neoplasms and the inflammatory cascade activation after lipopolysaccharide administration, even if their role remains not completely elucidated. Treatment of a cultured established glioma cell line (C6 rat astrocytoma cell line) induces a modification in the pattern of expression and of sub cellular distribution of PI‐PLCs compared to untreated cells. Special attention require PI‐PLC beta3 and PI‐PLC gamma2 isoforms, whose expression and sub cellular localization significantly differ after U‐73122 treatment. The meaning of these modifications is unclear, also because the use of this N‐aminosteroid compound remains controversial, inasmuch it has further actions which might contribute to the global effect recorded on the treated cells. J. Cell. Biochem. 110: 1005–1012, 2010. © 2010 Wiley‐Liss, Inc.