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Transglutaminase response during differentiation and apoptosis in myelogenous leukemia cells
Author(s) -
Miller Logan Tyler
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.943.17
Subject(s) - tissue transglutaminase , sodium butyrate , k562 cells , apoptosis , propidium iodide , retinoic acid , leukemia , chemistry , trypan blue , cellular differentiation , microbiology and biotechnology , cell culture , annexin , biochemistry , chronic myelogenous leukemia , programmed cell death , biology , immunology , enzyme , genetics , gene
Tissue transglutaminase (tTg) covalently modifies proteins by the formation between an ε‐amino group of a lysine residue and a γ‐carboxamide group of a glutamine residue. The expression of tTG is a widely used marker for apoptosis and cellular differentiation. The K562 cells, a myelogenous leukemia cell line, are differentiation‐incompetent, programmed cell death‐competent cancer cells. The objective of the study was to examine tTg response following exposure to chemicals known to induce differentiation and/or apoptosis. The K562 cells were treated with various chemicals including sodium butyrate and heteroarontinoids (HETS), retinoids with one aromatic ring and at least one heteroatom. The chemicals were introduced to cellular suspensions of K562 cells and McCoy's Modified 5a media. After 48 hours of exposure the cells were processed using trypan blue exclusion, Hoechst/propidium iodide assay, and a morphology evaluation from May Grunwald‐Giemsa stained cytospin slide preparations. The expression of tTg was evaluated using SDS‐PAGE Electrophoresis/Western Blotting. Preliminary results show that tissue transglutaminase is unresponsive to retinoic acid treatments. The heteroarotinoids showed varying levels of tissue transglutaminase expression as well as differing levels of apoptosis. Sodium butyrate effected the growth of K562 cells by decreasing the growth rate. Support was provided by SRU.