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Ethanol differentially affects metabolic and mitotic processes in chick embryonic cells
I A Shibley1, F M Carver, S N Pennington
1Department of Biochemistry, East Carolina University School of Medicine, Greenville, North Carolina, USA.
Abstract:
Our laboratory has been investigating the mechanisms by which ethanol-induced growth inhibition occurs in a developing embryo, and our studies have focused on disruption of cellular signaling pathways. Previous work on ethanol-induced changes in signaling systems that regulate ornithine decarboxylase activity indicated that the pathways containing protein kinase A, protein kinase C (PKC), and insulin-dependent tyrosine kinase were important for the control of ornithine decarboxylase in chick embryonic cells. Herein, we report ethanol's effect on the regulation of glucose uptake and thymidine uptake by these same kinase pathways. A pronounced increase in glucose uptake was associated with PKC downregulation in both vehicle- and ethanol-exposed cells, with the larger increase occurring in ethanol-exposed cells. An increase in thymidine uptake was associated with an activation of all three kinases, as well as with downregulation of PKC. Because previous work on signaling pathways has looked for changes in the insulin signaling pathway, the work herein focuses on the signaling pathways involving protein kinase A and PKC. cAMP levels were increased by ethanol treatment, but the increase was relatively small. Analysis of changes in PKC activity induced by ethanol exposure showed a significant suppression of PKC activity in the ethanol-treated cells and suggested that, overall, ethanol treatment affects the regulation of glucose uptake in embryonic cells predominantly by PKC downregulation.
Insights
Ethanol exposure in developing embryos disrupts cellular signaling pathways, significantly increasing glucose uptake primarily through protein kinase C (PKC) downregulation. This research highlights PKC
Area of Science:
- Developmental Biology
- Cellular Signaling
- Biochemistry
Background:
- Ethanol exposure during embryonic development can cause growth inhibition by disrupting cellular signaling pathways.
- Previous research identified protein kinase A, protein kinase C (PKC), and insulin-dependent tyrosine kinase pathways as crucial for regulating ornithine decarboxylase activity in chick embryonic cells.
Purpose of the Study:
- To investigate the effects of ethanol on glucose and thymidine uptake in embryonic cells.
- To elucidate the role of protein kinase A and PKC signaling pathways in ethanol-induced cellular changes.
Main Methods:
- Examined ethanol's impact on glucose and thymidine uptake in embryonic cells.
- Analyzed changes in protein kinase A and PKC activity and cyclic adenosine monophosphate (cAMP) levels following ethanol exposure.
Main Results:
- Ethanol exposure led to a pronounced increase in glucose uptake, strongly correlated with protein kinase C (PKC) downregulation.
- Increased thymidine uptake was observed with the activation of protein kinase A, protein kinase C, and insulin-dependent tyrosine kinase, alongside PKC downregulation.
- Ethanol treatment resulted in a significant suppression of PKC activity and a small increase in cAMP levels.
Conclusions:
- Ethanol disrupts embryonic cell regulation of glucose uptake predominantly through the downregulation of protein kinase C (PKC).
- The findings emphasize the critical role of PKC signaling in mediating ethanol's effects on embryonic development.