ArticleCellular and molecular neurobiology2022
Prostaglandin E2 Increases Neurite Length and the Formation of Axonal Loops, and Regulates Cone Turning in Differentiating NE4C Cells Via PKA.
Article in Cellular and molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Prostaglandin ESignal transduction and targeted therapy · 2026Article
- Emodin inhibits benzidine‑enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway.International journal of oncology · 2024Article
- Lipid-Based Molecules on Signaling Pathways in Autism Spectrum Disorder.International journal of molecular sciences · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E2 (PGE2) is a membrane-derived lipid signaling molecule important in neuronal development. Abnormal levels of PGE2, due to environmental insults prenatal development, have been linked to brain pathologies. We have previously shown that the addition of PGE2 to neuroectodermal (NE4C) stem cells affects early stages of neuronal differentiation (day 0-8) including increased stem cell motility, accelerated formation of neurospheres, and elevated calcium levels in growth cones. In this study, we further examine whether PGE2 can influence actin-dependent neuronal morphology in later stages (day 8-12) of NE4C cell differentiation. We show that exposure to PGE2 from the initiation of differentiation increased neurite length and the proportion of neurites that formed axonal loops. We also observed changes in the proportion of turning growth cones as the differentiation progressed, with a reduced likelihood of observing turning (or asymmetrical) growth cones on day 8 and increased odds on days 10 and 12. Moreover, we showed for the first time that the observed changes in cytoskeletal morphology were PGE2/PKA dependent. Interestingly, we also found that PGE2 decreased the total protein levels of the actin-bound form of spinophilin and increased levels of unbound PKA-phosphorylated ser94-spinophilin. Hence, we propose that exposure to PGE2 can destabilize the actin cytoskeleton at various stages of neuronal differentiation due to dissociation of ser94-spinophilin causing changes in neuronal morphology.
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