Ethanolamine requirement and cell proliferation

The hypothesis that ethanolamine deficiency alters the membrane phospholipid composition to such an extent that transduction of growth factor signals is inhibited was examined in two ethanolamine-responsive normal human cell lines, epidermal keratinocytes and mammary epithelial cells. Incubation of...

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Bibliographic Details
Main Author: Ashagbley, Anthony J.
Format: Others
Language:en
en_US
Published: 2007
Online Access:http://hdl.handle.net/1993/779
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Summary:The hypothesis that ethanolamine deficiency alters the membrane phospholipid composition to such an extent that transduction of growth factor signals is inhibited was examined in two ethanolamine-responsive normal human cell lines, epidermal keratinocytes and mammary epithelial cells. Incubation of keratinocytes and human mammary epithelial cells in media without ethanolamine resulted in a 55.2% and 53.1% reduction in cell proliferation respectively. Further studies with mammary epithelial cells showed that in the absence of ethanolamine in the growth medium, incorporation of ($\sp3$H) -thymidine into DNA was reduced by 5-fold. In keratinocytes, ethanolamine significantly enhanced the stimulatory effects of insulin and epidermal growth factor on DNA synthesis by 69% and 40.5% respectively. Insulin, in particular, was critical for the optimal proliferation of keratinocytes. Addition of ethanolamine to the growth media of mammary epithelial cells enabled a normal progression of cells through the cell cycle. In contrast, ethanolamine-deficient cells accumulated in the G0/G1 phase of the cell cycle. Ethanolamine but not dimethylethanolamine or monomethylethanolamine was mitogenic for quiescent ethanolamine-deficient cells. Proliferation of cells incubated in dimethylethanolamine and monomethylethanolamine was 55.5% and 47.2%, respectively, of cells incubated in ethanolamine-sufficient media. The incorporation of ($\sp3$H) -glycerol into phosphatidylethanolamine in ethanolamine-deficient keratinocytes and mammary epithelial cells was significantly reduced by 58.5% and 64.3%, respectively, compared to controls. The incorporation of ($\sp3$H) -glycerol into other glycerophospholipids in ethanolamine-sufficient and ethanolamine-deficient cells were unchanged. Insulin stimulation of quiescent keratinocytes and mammary epithelial cells in the presence of ethanolamine activated mitogen-activated protein kinase. (Abstract shortened by UMI.)