title: Expression of three major protein kinase C isozymes in various types of human leukemic cells.
abstract: We examined the levels of protein kinase C (PKC) activity and the expressions of its three major isozymes, designated types I (gamma), II (beta), and III (alpha), in the cytosol and particulate fractions of cells from patients with acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), and chronic lymphocytic leukemia (CLL), in an attempt to elucidate the cell type- or lineage-specific expression of these isozymes. The levels of PKC activities in the cytosol and particulate fractions from AML cells were higher than those from ALL or CLL cells. The average PKC activities of AML cells, ALL cells, and CLL cells were 18.7, 12.2, and 11.3 pmol/min/10(8) cells, respectively, in the cytosol fractions and 4.4, 3.1, and 2.6 pmol/min/10(8) cells, respectively, in their particulate fractions. M1 cells (French-American-British classification) and AML cells with T-lymphocyte-associated surface antigens, such as CD2 and CD7, had significantly lower PKC activities among AML cells. Immunoblot analyses using monoclonal antibodies against each isozyme revealed that all three isozymes were broadly distributed on leukemic cells with considerable variability in the level of expression. All lymphoid leukemic cells expressed PKC-gamma in the cytosol fractions, albeit a minor component; however, this type was observed in cells from only half the number of AML patients. Those AML cells with cytosolic PKC-gamma usually expressed lymphoid surface antigens, such as CD2, CD7, and CD19. On the other hand, cytosolic PKC-beta and PKC-alpha were commonly observed in all types of leukemic cells. AML cells expressed these two types at almost equal levels, but in lymphoid cells, expressions of PKC-beta were usually more abundant than those of PKC-alpha. These data suggest that AML cells with lymphoid antigens might have a lower PKC activity but more predominant expression of cytosolic PKC-gamma than the usual AML cells.
authors.affiliation: Department of Internal Medicine, Mie University School of Medicine, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Komada
authors.forename: M
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Uemura
authors.forename: K
authors.initials: K
authors.lastname: Morita
authors.forename: H
authors.initials: H
authors.lastname: Hidaka
authors.forename: S
authors.initials: S
authors.lastname: Shirakawa
mesh_terms: D000328:Adult; D003600:Cytosol / Q000201:enzymology; D006801:Humans; D015151:Immunoblotting; D016130:Immunophenotyping; D007527:Isoenzymes / Q000302:isolation & purification / Q000378:metabolism*; D007700:Kinetics; D007938:Leukemia / Q000201:enzymology* / Q000276:immunology; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000201:enzymology; D015470:Leukemia, Myeloid, Acute / Q000201:enzymology; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000201:enzymology; D011493:Protein Kinase C / Q000302:isolation & purification / Q000378:metabolism*
chemical_list: D007527:Isoenzymes; D011493:Protein Kinase C