Prostaglandin E(2) and misoprostol induce neurite retraction in Neuro-2a cells.

Abstract

Prostaglandin E(2) (PGE(2)) is a key lipid-derived compound which mediates important physiological functions in the nervous system via activation of four EP receptors (EP1-4). Recent studies have shown that altered PGE(2) signalling due to abnormal lipid peroxidation and oxidative stress may underlie some pathologies of the nervous system. The prenatal exposure to the drug misoprostol, a prostaglandin type E analogue, has also been linked to a number of neurodevelopmental defects. In the present study, we use ratiometric calcium imaging with fura-2AM as a calcium indicator to determine the effects of PGE(2) and misoprostol on calcium homeostasis in growth cones of mouse neuroblastoma (Neuro-2a) cells. Our results show that both drugs increase the amplitude of calcium transients in growth cones of Neuro-2a cells and induce neurite retraction. Moreover, quantitative real-time PCR also revealed that the mRNA expression level of the four EP receptors was significantly higher during the neurogenesis period in mouse indicating the importance of PGE(2) signalling in the nervous system.

• Authors: Javaneh Tamiji, Dorota A Crawford
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 398 Issue 3 Pg. 450-6 (Jul 30 2010) ISSN: 1090-2104 [Electronic] United States
• PMID: 20599704 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Crown Copyright 2010. Published by Elsevier Inc. All rights reserved.

Chemical References

• Fluorescent Dyes
• RNA, Messenger
• Receptors, Prostaglandin E
• Misoprostol
• fura-2-am
• Dinoprostone
• Calcium
• Fura-2

Topics

• Animals
• Brain (drug effects, metabolism)
• Calcium (metabolism)
• Cell Line, Tumor
• Dinoprostone (pharmacology)
• Fluorescent Dyes (metabolism)
• Fura-2 (analogs & derivatives, metabolism)
• Growth Cones (drug effects, metabolism)
• Mice
• Misoprostol (pharmacology)
• Neurites (drug effects, metabolism, physiology)
• Neurogenesis (drug effects)
• RNA, Messenger (biosynthesis, genetics)
• Receptors, Prostaglandin E (biosynthesis, genetics)