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An ethanol‐sensitive variant of the PC12 neuronal cell line: Sensitivity to alcohol is associated with increased cell adhesion and decreased glucose accumulation
Author(s) -
Dwyer Donard S.,
Liu Ye,
Bradley Ronald J.
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199901)178:1<93::aid-jcp12>3.0.co;2-u
Subject(s) - ethanol , alcohol , sensitivity (control systems) , cell culture , cell adhesion , chemistry , cell , adhesion , microbiology and biotechnology , biophysics , biochemistry , biology , genetics , organic chemistry , electronic engineering , engineering
A stable variant of the PC12 cell line (PC12.4) has been isolated on the basis of its cell adhesive properties and morphological characteristics. Cells from the PC12.4 subline differ from the parental cell line in that they readily adhere to untreated plastic surfaces and grow individually rather than aggregated in large clusters. When compared to the PC12.1 cell line (original phenotype), PC12.4 cells were found to have a more rapid growth rate (24 h vs. 40 h doubling time) and higher production of lactate but lower glucose metabolism as judged by the accumulation of 3 H‐2‐deoxyglucose. Western blot analyses also revealed differences between PC12.1 and PC12.4 cells with respect to the expression of glucose transporters (GLUTs) and the subcellular distribution of the heat shock protein (Hsp) Hsp60. We have reported here that PC12.4 cells were far more sensitive to growth inhibition by ethanol when compared with PC12.1 cells and appeared to be more dependent upon glutamine and serum for cell growth. The cytostatic effects of ethanol were most pronounced when the cells were cultured in medium with low concentrations of serum and glutamine. Thus, there appears to be an interplay between energy metabolism in the cell and the response to ethanol. J Cell Physiol 178:93–101, 1999. © 1999 Wiley‐Liss, Inc.